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Residential Proximity to Major Roadways and Renal Function
Abstract
Background:
Living near major roadways has been associated with increased risk of cardiovascular events, but little is known about its impact on renal function.
Methods:
We calculated the estimated glomerular filtration rate (eGFR) for 1103 consecutive Boston-area patients hospitalised with confirmed acute ischaemic stroke between 1999 and 2004. We used linear regression to evaluate the association between eGFR and categories of residential distance to major roadway (0 to ≤50, >50 to ≤100, >100 to ≤200, >200 to ≤400, >400 to ≤1000 and >1000 m) adjusting for age, sex, race, smoking, comorbid conditions, treatment with ACE inhibitor and neighbourhood-level socioeconomic characteristics. In a second analysis, we considered the log of distance to major roadway as a continuous variable.
Results:
Patients living closer to a major roadway had lower eGFR than patients living farther away (Ptrend=0.01). Comparing patients living 50 m versus 1000 m from a major roadway was associated with a 3.9 ml/min/1.73 m(2) lower eGFR (95% CI 1.0 to 6.7; p=0.007): a difference comparable in magnitude to the reduction in eGFR observed for a 4-year increase in age in population-based studies. The magnitude of this association did not differ significantly across categories of age, sex, race, history of hypertension, diabetes or socioeconomic status.
Conclusions:
Living near a major roadway is associated with lower eGFR in a cohort of patients presenting with acute ischaemic stroke. If causal, these results imply that exposures associated with living near a major roadway contribute to reduced renal function, an important risk factor for cardiovascular events.
... Several studies reported on the levels of particulate matters in relation to the glomerular filtration rate estimated from serum creatinine (eGFR) [4][5][6][7] , glomerulopathy 8 , prevalent 6 or incident 9 CKD, progression to end-stage renal disease 9 , microalbuminuria 10 , and the risk of renal cancer in relation to air pollutants 11 . These studies enrolled population samples 10,11 , stroke patients 4 , or older male veterans 5,7,9 . ...
... Other reports focused on coarse particulate 6 . Of the eight reviewed studies [4][5][6][7][8][9][10][11] , none reported on BC exposure. To address this knowledge gap, we analysed data from The Flemish Study on Environment, Genes and Health Outcomes (FLEMENGHO 12 ). ...
... Patients living at a distance of 50 m vs. 1 kilometre had a 3.9 mL/min/1.73 m 2 lower eGFR (P = 0.007) 4 . ...
Whereas the adverse impact of fine particulate matter on coronary heart disease and respiratory disorders has been clarified, its influence on glomerular function is not well defined in population studies. Serum creatinine levels were quantified in 820 randomly recruited people (50.7% women; mean age 51.1 years). Among them, 653 participants were followed up for a median of 4.8 years. Using multivariable-adjusted mixed model, eGFR (or serum creatinine) both at baseline and follow-up were regressed against long term residential black carbon (BC) or PM2.5 (particles with an aerodynamic diameter ≤2.5 µm). In longitudinal analysis, the percent change in eGFR was regressed against long term residential exposure to BC or PM2.5. eGFR averaged 80.9 (SD 16.4) mL/min/1.73m2 and median long term PM2.5 and black carbon amounted 13.1 (SD 0.92) and 1.10 (SD 0.19) µg/m³, respectively. In multivariable-adjusted cross-sectional analyses, eGFR was unrelated to BC and PM2.5 (P ≥ 0.59). During follow-up, eGFR decreased on average by 1.9 mL/min/1.73m2 (95% confidence interval: 1.0-2.8). The percentage decline in eGFR was not significantly associated with either BC or PM2.5 (P ≥ 0.75). In conclusion, long-term residential exposure to PM2.5 and black carbon is not associated with eGFR decline in predominantly healthy people drawn from a general semirural population.
... Because renal hemodynamics are closely related to blood pressure, vascular reactivity, and endothelial function, renal function might be in uenced by noise-induced stress 13 . One study showed that residential proximity to major roadways is related to the reduction of renal function in hospitalized patients with acute ischemic stroke 14 . In addition, a reduction in renal function has been associated with community noise exposure in male patients with cardiovascular disease 15 . ...
... There have been few studies on the relationship between noise and renal function. Epidemiological research in 1,103 patients-from the Boston area, United States-with ischemic stroke showed lower eGFR for those living closer to a major roadway 14 . In 217 patients with cardiovascular heart disease, increased exposure to day-evening-night noise levels (L den ) resulted in a decrease in eGFR among males who experienced ischemic heart disease or stroke and who were exposed to lower air pollution 15 . ...
Exposure to occupational and environmental noise is closely linked to various diseases of auditory system. Few studies have focused on noise exposure effect on extra auditory system especially, urinary system. This study analyzed 17,202 participants aged 40–79 years from the Korea National Health and Nutrition Examination Survey between 2013 and 2018. A self-reported questionnaire was used to assess occupational or environmental noise exposure. Logistic regression was used to determine the differences in chronic kidney disease (CKD) prevalence considering noise exposure characteristics. For participants with noise exposure, linear regression was performed to determine the noise exposure period and estimated glomerular filtration rate (eGFR). In the noise exposure group, a higher CKD prevalence was associated with females who experienced long-term occupational noise (≥ 240 months), compared with the other groups (Adjusted OR = 2.86, 95% CI: 1.18–6.94). An increase of one month of occupational noise exposure was associated with a 0.0096 mL/min/1.73 m ² , 0.0080 mL/min/1.73 m ² , and 0.0159 mL/min/1.73 m ² decrease of eGFR in total, in males, and in females, respectively. Our results suggest that noise exposure can be a risk factor for reduced renal function, especially long-term exposure to occupational noise. More precise studies are necessary to determine the relationship between noise and renal function and the underlying mechanisms.
... A growing body of epidemiological research has reported associations between long-term exposure to PM 2.5 and a variety of renal disease outcomes. [10][11][12][13][14] For example, Mehta et al 13 observed that long-term exposure to PM 2.5 led to kidney function decline with a lower estimated glomerular filtration rate (eGFR). Bowe et al 14 demonstrated positive associations between long-term exposure to PM 2.5 and increased risks of incident chronic kidney disease (CKD), eGFR decline, and end-stage renal disease (ESRD). ...
... 51 Second, as the kidney is a vascularized organ, biological hypotheses related to the associations between PM 2.5 exposure and cardiovascular disease outcomes may also be pertinent to kidney disease outcomes. 10,14,52 One possibility is that fine particle-induced disturbances in the pulmonary nervous system could affect the function of the heart, causing congestion of blood in kidneys. 52 Another possibility is that fine particles entering the bloodstream would directly interact with the kidney vasculature to promote the decline of kidney function. ...
Background:
Toxicological evidence has shown that fine particulate matter (PM2.5) may affect distant organs, including kidneys, over the short term. However, epidemiological evidence is limited.
Objectives:
We investigated associations between short-term exposure to PM2.5, major PM2.5 components [elemental carbon (EC), organic carbon (OC), sulfate, and nitrate], and gaseous co-pollutants (O3, CO, SO2, NO2, and NOx) and emergency department (ED) visits for kidney diseases during 2002–2008 in Atlanta, Georgia.
Methods:
Log-linear time-series models were fitted to estimate the acute effects of air pollution, with single-day and unconstrained distributed lags, on rates of ED visits for kidney diseases [all renal diseases and acute renal failure (ARF)], controlling for meteorology (maximum air and dew-point temperatures) and time (season, day of week, holidays, and long-term time trend).
Results:
For all renal diseases, we observed positive associations for most air pollutants, particularly 8-day cumulative exposure to OC [rate ratio (RR) = 1.018, (95% confidence interval [CI]: 1.003, 1.034)] and EC [1.016 (1.000, 1.031)] per interquartile range increase exposure. For ARF, we observed positive associations particularly for 8-day exposure to OC [1.034 (1.005, 1.064)], EC [1.032 (1.002, 1.063)], nitrate [1.032 (0.996, 1.069)], and PM2.5 [1.026 (0.997, 1.057)] per interquartile range increase exposure. We also observed positive associations for most criteria gases. The RR estimates were generally higher for ARF than all renal diseases.
Conclusions:
We observed positive associations between short-term exposure to fine particulate air pollution and kidney disease outcomes. This study adds to the growing epidemiological evidence that fine particles may impact distant organs (e.g., kidneys) over the short term.
... PM 2.5 can induce systemic-wide effects through mechanisms involving inflammation, oxidation, and direct toxicity from particle constituents [13,14]. In animal models, inhalation of diesel exhaust has been shown to induce renal oxidative stress, inflammation, and DNA damage, while a 6-year study of Boston hospital stroke patients found that individuals living closer to roadways showed reduced renal function [15,16]. On a global scale, Bowe et al. estimated that PM 2.5 can be attributed to 17-20% of CKD burden with an estimated 6.95 million annual cases caused by PM 2.5 exposure [8]. ...
... Conversely, the association between PM 2.5 and CKD prevalence and eGFR in cross-sectional studies is unclear. Blum et al. [18] found no significant association between baseline PM 2.5 and eGFR 16 , which differed from our results indicating an association between annual PM 2.5 and prevalent CKD, eGFR <45 ml/min/1.73 m 2 (18% greater odds). ...
Recent evidence has shown that fine particulate matter (PM2.5) may be an important environmental risk factor for chronic kidney disease (CKD), but few studies have examined this association for individual patients using fine spatial data.
To investigate the association between PM2.5 and CKD (estimated glomerular filtration rate [eGFR]<45 ml/min/1.73 m²) in the Twin-Cities area in Minnesota using a large electronic health care database (2012–2019).
We estimated the previous 1-year average PM2.5 from the first eGFR (measured with the CKD Epidemiology Collaboration equation using the first available creatinine measure during the baseline period [2012–2014]) using Environmental Protection Agency downscaler modeling data at the census tract level. We evaluated the spatial relative risk and clustering of CKD prevalence using a K-function test statistic. We assessed the prevalence ratio of the PM2.5 association with CKD incidence using a mixed effect Cox model, respectively.
Patients (n = 20,289) in the fourth (PM2.5 > 10.4), third (10.3 < PM2.5 < 10.8) and second quartile (9.9 < PM2.5 < 10.3) vs. the first quartile (<9.9 μg/m³) had a 2.52[2.21, 2.87], 2.18[1.95, 2.45], and 1.72[1.52, 1.97] hazard rate of developing CKD in the fully adjusted models, respectively. We identified spatial heterogeneities and evidence of CKD clustering across our study region, but this spatial variation was accounted for by air pollution and individual covariates.
Exposure to higher PM2.5 is associated with a greater risk for incident CKD. Improvements in air quality, specifically at hotspots, may reduce CKD.
... Apart from mortality, exposure to PM 2.5 has been found to increase the risk of vascular inflammation and atherosclerosis (Brook et al. 2010;Hoffmann et al., 2009;Nemmar et al., 2016), and it is widely accepted that PM 2.5 exerts detrimental effects on the development and progression of cardiovascular disease (CVD) (Brook et al., 2010;Lin et al., 2018). As a highly vascularized organ, kidney might also be susceptible to PM-related small vessel dysfunction and large vessel atherosclerosis (Lue et al., 2013). ...
... Apart from the immunoregulation, some studies also suggested that hemodynamic pathways may also contribute to the associations between PMs and eGFR, as exposure to PMs may impair the vascular tone control, mediating diastolic blood pressure, reducing renal blood flow, and then contribute to the chronic renal insufficiency (Al Suleimani et al., 2017;Mehta et al., 2016). Previous study also hypothesizes that the associations between PMs and eGFR are possibly mediated by pathways associated with PM-related vascular/endothelial dysfunction (Lue et al., 2013). However, we found the PM 2.5 -related difference of Scr and eGFR narrowed with the increasing proportion of PM 1 included in PM 2.5 . ...
Background
Limited studies have examined the impact of airborne particulate matter of 2.5 μm or less (PM2.5) on renal function. No study has examined the effect of PM1, which is small enough to reach the blood circulation. We examined whether exposure to PM1 or PM2.5 affected renal function of young Han Chinese.
Method
We included 2,546,047 young adults who were aged 18 to 45 years, being Han ethnicity and had no chronic disease from a Chinese national birth cohort. Serum creatinine (Scr) of each participant was measured during the baseline examination. Estimated glomerular filtration rate (eGFR) were calculated for each participant using the latest Chronic Kidney Disease Epidemiology Collaboration equation. One-year average exposure to PM1 and PM2.5 prior to the health examination for each participant were estimated using machine learning models with satellite remote sensing information. Generalized additive mixed models were used to estimate associations between PM1 or PM2.5 and renal function after adjusting for detailed individual variables.
Results
A 10 μg/m³ increment in PM1 exposure was associated with −0.95% (95%CI: −1.04%, −0.87%) difference of eGFR in females and −0.37% (95%CI: −0.44%, −0.31%) in males. For PM2.5, the corresponding difference of eGFR was −0.99% (95%CI: −1.05%, −0.93%) in females and −0.48% (95%CI: −0.53%, −0.43%) in males, respectively. Associations between eGFR and PM were higher in females compared to males (p < 0.05 for interaction test). Association with PM1 were weaker than that with other fractions included in PM2.5. Participants who worked as farmers, were of normal weight, were not exposed to tobacco smoking, did not drink alcohol, had higher associations between eGFR and PM than their counterparts (p < 0.05 for interaction test).
Conclusion
Exposure to PM1 and PM2.5 was associated with reduced renal function among Han Chinese at reproductive age.
... We adjusted for the following confounders in all multivariate linear regression models: MA (< 35 or ≥ 35 years), race (the Han nationality or national minority), parity (nulliparous or multiparous), pre-pregnancy BMI (continuous), pregnancy-associated hypertensive disorders (yes or no), GDM (yes or no), gestational age (GA) at the time of renal function test (continuous), seasons of renal function test (Spring, form March 1 to April 31; Summer, form June 1 to August 31; Autumn, from September 1 to November 30; Winter, form December 1 to February 30). Those confounders were chosen according to the data accessibility and their potential associations with renal function or PM 2.5 exposure (Chan et al., 2018;Lue et al., 2013;Mehta et al., 2016). The linear regression model assumptions of normality, constancy of variance and linearity were assessed by examining standard residual-based plots and were fulfilled for the finial linear regression models. ...
... The mechanisms through which PM 2.5 exposure exerts its adverse effects on renal function are not clear. Kidney is a highly vascularized organ and susceptible to microvascular dysfunction and atherosclerotic disease (Lue et al., 2013). It is well recognized that PM 2.5 exposure could lead to oxidative stress, systemic inflammation and atherosclerosis (Bai and Sun 2016;Weichenthal et al., 2013), which might induce vascular dysfunction and result in microvascular damage and atherosclerotic disease. ...
Background
Fine particulate matter (PM2.5) is the most serious environmental threat worldwide. The nephrotoxicity of PM2.5 has been demonstrated in older adults, but no study has addressed the impacts of PM2.5 exposure on renal function in pregnant women, who are recognized to be vulnerable and susceptible to PM2.5 exposure.
Objective
To evaluate whether exposures to PM2.5 total mass and its chemical constituents were associated with reduced renal function among pregnant women in China.
Methods
We measured serum concentrations of urea nitrogen (UN), uric acid (UA) and creatinine for 10,052 pregnant women in Shanghai, China. Exposures to PM2.5 total mass and its 5 key chemical constituents during the whole pregnancy and each trimester of pregnancy was represented by satellite-based models.
Results
Exposures to PM2.5 total mass and its chemical constituents of organic matter (OM), black carbon (BC), nitrate (NO3⁻) and ammonium (NH4⁺) were positively associated with serum levels of UN and UA, and negatively associated with estimated glomerular filtration rate (eGFR). An interquartile rang (IQR) increase in PM2.5 total mass, OM, BC, NO3– and NH4⁺ exposure in third trimester was associated with 1.33 (β = -1.33, 95% CI, −1.79, −0.87), 1.67 (β = -1.67, 95% CI, −2.26, −1.07), 1.29 (β = -1.29, 95% CI,-1.89, −0.70), 1.16 (β = -1.16, 95% CI,-1.66, −0.65) and 0.76 (β = -0.76, 95% CI, −1.08, −0.44) mL/min/1.73 m² decrease in eGFR, respectively.
Conclusion
We concluded that exposures to PM2.5 during pregnancy were associated with decreased renal function among pregnant women.
... The involvement of polycyclic aromatic hydrocarbons and benzo(α)pyrenes accompanying NO 2 in vehicle emissions has also been suggested [47]. Chronic kidney disease, which has been observed in individuals exposed to particulate matter [48][49][50][51], is also associated with kidney and bladder cancer recurrence and progression [52,53]. These findings suggest that exposure to air pollutants could contribute to a vicious circle favoring the onset of chronic kidney disease, itself a risk factor for kidney cancer. ...
Background
Although several risk factors of kidney cancer have already been well-addressed, many remain underappreciated, such as chronic exposure to air pollution. This systematic review and meta-analysis aims to assess the association between air pollutant exposure and the risk of kidney cancer.
Methods
With an exhaustive search equation including keywords related to air pollution and kidney cancer on EMBASE, PubMed, Web of science, Cochrane Library and CINAHL database, we identified all relevant articles published before March 23rd, 2023 (Prospero registration number: CRD42020187956). Using random-effects meta-analysis, we present pooled hazard ratios (with their respective 95% confidence interval) associated with a 10 µg/m ³ increase in each pollutant level. Heterogeneity was quantified by the I 2 statistic. Risks of methodological and publication bias were also both assessed using appropriate tools.
Results
Of the 1919 records identified, our review included 19 articles (13 cohort, 5 registry-based and 1 case–control studies), of which 9 were suitable for the meta-analysis. We found a significantly increased risk of kidney cancer incidence for a 10 μg/m ³ elevation of both particulate matter of less than 10 µm (PM 10 ) (HR = 1.29 [1.10; 1.51], I ² = 0%, p = 0.002) and nitrogen dioxide (NO 2 ) (HR = 1.10 [1.03; 1.18], I ² = 20%, p = 0.004). Secondary analyses also suggest an increased risk of kidney cancer-related morbidity-mortality associated with PM 10 exposure.
Conclusions
Overall, our findings suggest a potential association between exposure to increased levels of PM 10 and NO 2 and the risk of kidney cancer. These results should nonetheless be interpreted with caution due to the limited number of included studies and their significant risk of methodological bias.
Graphical abstract
... Furthermore, Chen et al. observed a positive correlation between cumulative noise exposure and mild renal impairment in petrochemical workers [45]. Lue et al. also found that noise was associated with a lower eGFR in B6C3F1 mice [46]. Prolonged exposure to noise induces a stress response that activates the sympathetic and endocrine systems, escalating oxidative stress, triggering pro-oxidase enzymes, and leading to an excess of ROS in the kidneys. ...
Background
Chronic kidney disease (CKD) carries a high public health burden yet little is known about the relationship between metalworking fluid (MWF) aerosols, occupational noise and CKD. We aimed to explore the relationship between occupational MWF aerosols, occupational noise and CKD.
Methods
A total of 2,738 machinists were sampled from three machining companies in Wuxi, China, in 2022. We used the National Institute for Occupational Safety and Health (NIOSH) method 5524 to collect individual samples for MWF aerosols exposure, and the Chinese national standard (GBZ/T 189.8–2007) method to test individual occupational noise exposure. The diagnostic criteria for CKD were urinary albumin/creatinine ratio (UACR) of ≥ 30 mg/g and reduced renal function (eGFR < 60 mL.min− 1. 1.73 m− 2) lasting longer than 3 months. Smooth curve fitting was conducted to analyze the associations of MWF aerosols and occupational noise with CKD. A segmented regression model was used to analyze the threshold effects.
Results
Workers exposed to MWF aerosols (odds ratio [OR] = 2.03, 95% confidence interval [CI]: 1.21–3.41) and occupational noise (OR = 1.77, 95%CI: 1.06–2.96) had higher prevalence of CKD than nonexposed workers. A nonlinear and positive association was found between increasing MWF aerosols and occupational noise dose and the risk of CKD. When daily cumulative exposure dose of MWF aerosols exceeded 8.03 mg/m³, the OR was 1.24 (95%CI: 1.03–1.58), and when occupational noise exceeded 87.22 dB(A), the OR was 1.16 (95%CI: 1.04–1.20). In the interactive analysis between MWF aerosols and occupational noise, the workers exposed to both MWF aerosols (cumulative exposure ≥ 8.03 mg/m³-day) and occupational noise (LEX,8 h ≥ 87.22 dB(A)) had an increased prevalence of CKD (OR = 2.71, 95%CI: 1.48–4.96). MWF aerosols and occupational noise had a positive interaction in prevalence of CKD.
Conclusions
Occupational MWF aerosols and noise were positively and nonlinearly associated with CKD, and cumulative MWF aerosols and noise exposure showed a positive interaction with CKD. These findings emphasize the importance of assessing kidney function of workers exposed to MWF aerosols and occupational noise. Prospective and longitudinal cohort studies are necessary to elucidate the causality of these associations.
... On the basis of previous studies [26][27][28], we categorized potential confounders into three sets: demographic features, health-related behaviors and metrics, diseases and air pollution-related data. Demographic features included age, sex, marital status (currently married and living with spouse, separated/divorced/never married, or widowed), years of education (0, 1-6, and > 6 years), and residence (rural vs. urban). ...
Background
With rapid urban sprawl, growing people are living in the vicinity of major roadways. However, little is known about the relationship between residential proximity to major roadways and hearing impairment (HI).
Methods
We derived data from the 2018 wave of the Chinese Longitudinal Healthy Longevity Survey, and included 13,775 participants aged 65 years or older. Multivariate logistic regressions were employed to examine the association between residential proximity to major roadways and HI. The effects of corresponding potentially modifiable factors were studied by three-way interaction analyses. Sensitivity analyses were performed to verify the robustness of the results.
Results
The prevalence of HI was 38.3%. Participants living near major roadways were more likely to have a higher socioeconomic status. An exposure-response relation between residential proximity to major roadways and HI was observed ( P trend < 0.05). Compared with individuals living > 300 m away from major roadways, the adjusted odds ratios (OR) were 1.07 (95% CI: 0.96–1.24), 1.15 (95% CI: 1.07–1.34), and 1.12 (95% CI: 1.01–1.31) for those living 101–200 m, 50–100 m, and < 50 m away from the roadways, respectively. Particularly, the association was more pronounced among individuals exposed to carbon monoxide (CO) pollution or opening windows frequently ( P interaction < 0.05). Three-way interaction analyses confirmed that participants exposed to CO pollution and frequently leaving windows open had the highest OR of 1.73 (95% CI: 1.58–1.89).
Conclusions
This nation-wide cohort study suggested that residential proximity to major roadways was significantly associated with an increased exposure-response risk of HI in Chinese older adults. Exposure to CO pollution and opening windows frequently might strengthen the relations.
... In addition, studies addressing modelled BC exposure and eGFR are scarce (Gao et al., 2019;Zhao et al., 2020), and no personalized BC exposure data has been linked to a decline in eGFR before. In the Boston area, Lue et al. (Lue et al., 2013) observed that ischemic stroke patients who lived within 50 m from a major road had a 3.9 (95 % CI 1.0 to 6.7) mL/min/ 1.73 m 2 lower eGFR (p < 0.01) compared to those living further than 1000 m from a major road. In another study performed by the same research group, a similar trend was shown, where a decrease of 1.4 (95 % CI − 4.7 to 2.0) mL/min/1.73 ...
Background: Ultrafine particles, including black carbon (BC), can reach the systemic circulation and therefore may distribute to distant organs upon inhalation. The kidneys may be particularly vulnerable to the adverse effects of BC exposure due to their filtration function. Objectives: We hypothesized that BC particles reach the kidneys via the systemic circulation, where the particles may reside in structural components of kidney tissue and impair kidney function. Methods: In kidney biopsies from 25 transplant patients, we visualized BC particles using white light generation under femtosecond-pulsed illumination. The presence of urinary kidney injury molecule-1 (KIM-1) and cystatin c (CysC) were evaluated with ELISA. We assessed the association between internal and external exposure matrices and urinary biomarkers using Pearson correlation and linear regression models. Results: BC particles could be identified in all biopsy samples with a geometric mean (5th, 95th percentile) of 1.80 × 103 (3.65 × 102, 7.50 × 103) particles/mm3 kidney tissue, predominantly observed in the interstitium (100 %) and tubules (80 %), followed by the blood vessels and capillaries (40 %), and the glomerulus (24 %). Independent from covariates and potential confounders, we found that each 10 % higher tissue BC load resulted in 8.24 % (p = 0.03) higher urinary KIM-1. In addition, residential proximity to a major road was inversely associated with urinary CysC (+10 % distance: −4.68 %; p = 0.01) and KIM-1 (+10 % distance: −3.99 %; p
... Existing studies have suggested some possible mechanisms. First, the kidney is a highly vascularized organ, susceptible to vascular dysfunction (Lue et al., 2013). Second, previous experiments have shown that inhaled particulate matter could enter the bloodstream through the alveolar and ultimately be excreted through the kidneys. ...
Previous research has implicated PM2.5 as a potential environmental risk factor for CKD, but little is known about the associations between its components and CKD. We conducted a nationwide cross-sectional study using the updated air pollution data in the nationwide population (N = 2,938,653). Using generalized additive models, we assessed the association between long-term exposure to PM2.5 and its components (i.e., black carbon [BC], organic matter [OM], nitrate [NO3-], ammonium [NH4+], sulfate [SO42-]), and CKD prevalence. The air pollution data was estimated using high-resolution and high-quality spatiotemporal datasets of ground-level air pollutants in China. Besides, we adopted a novel quantile-based g-computation approach to assess the effect of a mixture of PM2.5 constituents on CKD prevalence. The average concentration of PM2.5 was 78.67 ± 22.5 μg/m3, which far exceeded WHO AQG. In the fully adjusted generalized additive model, at a 10 km × 10 km spatial resolution, the ORs per IQR increase in previous 1-year average PM2.5 exposures was 1.380 (95%CI: 1.345-1.415), for NH4+ was 1.094 (95%CI: 1.062-1.126), for BC was 1.604 (95%CI: 1.563-1.646), for NO3- was 1.094 (95%CI: 1.060-1.130), for SO42- was 1.239 (95%CI: 1.208-1.272), and for the OM was 1.387 (95%CI: 1.354-1.421), respectively. Subgroup analysis showed females, younger, and healthier were more vulnerable to this effect. In the further exploration of the joint effect of PM2.5 compositions (OR 1.234 [95%CI 1.222-1.246]) per quartile increase in all 5 PM2.5 components, we found that PM2.5SO42- contributed the most. These findings provide important evidence for the positive relationship between long-term exposure to PM2.5 and its chemical constituents and CKD prevalence in a Chinese health check-up population, and identified PM2.5SO42- has the highest contribution to this relationship. This study provides clinical and public health guidance for reducing specific air particle exposure for those at risk of CKD.
... Recent studies confirmed an increased risk of breast cancer with vehicular-specific PM exposure among African American and Japanese American women living near major roads, highlighting the link between environmental injustice and health disparities (Cheng et al., 2020;Niehoof et al., 2020). Indeed, residential proximity to major roadways is a recognized risk factor beyond breast cancer, in cardiovascular disease (Hart et al., 2014;Kirwa et al., 2014;Kingsley et al., 2015;Kubil et al., 2018) and renal disease (Lue et al., 2013). Further, it disproportionately impacts racial and ethnic minoritized groups and those of lower socioeconomic status, the legacy of the widespread practice of redlining in the United States (Hwa Jung et al., 2022;Swope et al., 2022). ...
Activation of the aryl hydrocarbon receptor (AhR) through environmental exposure to chemicals including polycyclic aromatic hydrocarbons (PAHs) and polychlorinated dibenzo-p-dioxins (PCDDs) can lead to severe adverse health effects and increase the risk of breast cancer. This review considers several mechanisms which link the tumor promoting effects of environmental pollutants with the AhR signaling pathway, contributing to the development and progression of breast cancer. We explore AhR’s function in shaping the tumor microenvironment, modifying immune tolerance, and regulating cancer stemness, driving breast cancer chemoresistance and metastasis. The complexity of AhR, with evidence for both oncogenic and tumor suppressor roles is discussed. We propose that AhR functions as a “molecular bridge”, linking disproportionate toxin exposure and policies which underlie environmental injustice with tumor cell behaviors which drive poor patient outcomes.
... Finally, we acknowledge that the health effects from pollution and climate change are differentially distributed among communities in the United States and the world according to wealth/race/ethnicity (102), subjecting analyses to potential confounding and bias, and often limiting the ability to investigate associations in some subgroups. For example, distance to major roads, a proxy indicator for exposure to traffic-related air pollution and community wealth, are inversely associated with estimated GFR (103). Adequate attention to these issues and increased focus on vulnerable communities are needed to better understand the synergy of inequality and environmental exposures in the morbidity of kidney disease. ...
Accumulating evidence underscores the large role played by the environment in the health of communities and individuals. We review the currently known contribution of environmental exposures and pollutants on kidney disease and its associated morbidity. We review air pollutants, such as particulate matter; water pollutants such as trace elements, per- and polyfluorooakyl substances, and pesticides; and extreme weather events and natural disasters. We also discuss gaps in the evidence which at present relies heavily on observational studies and animal models, and propose using recently developed quantitative methods to help bridge the gaps. With the expected increase in the intensity and frequency of many environmental exposures in the decades to come, an improved understanding of their potential effect on kidney disease is crucial to mitigate potential morbidity and mortality.
... Exposure to particulate matter <2.5 μm (PM 2.5 ) increases mortality as well as the risk of vascular inflammation and atherosclerosis [6][7][8] and it is widely believed that PM 2.5 adversely affects the development and progression of cardiovascular disease [6,9]. The kidney, a highly vascularized organ, may also be susceptible to PM-related small vessel dysfunction and large vessel atherosclerosis [10]. ...
Background
Fuzzy inference systems (FISs) based on fuzzy theory in mathematics were previously applied to infer supplementary points for the limited number of monitoring sites and improve the uncertainty of spatial data. Therefore we adopted the FIS method to simulate spatiotemporal levels of air pollutants [particulate matter <2.5 μm (PM2.5), sulfur dioxide (SO2) and (NO2)] and investigated the association of levels of air pollutants with the community-based prevalence of chronic kidney disease (CKD).
Methods
A Complex Health Screening program was launched during 2012–2013 and a total of 8284 community residents in Chiayi County, which is located in southwestern Taiwan, received a series of standard physical examinations, including measurement of estimated glomerular filtration rate (eGFR). CKD cases were defined as eGFR <60 mL/min/1.73 m2 and were matched for age and gender in a 1:4 ratio of cases:controls. Data on air pollutants were collected from air quality monitoring stations during 2006–2016. The longitude, latitude and recruitment month of the individual case were entered into the trained FIS. The defuzzification process was performed based on the proper membership functions and fuzzy logic rules to infer the concentrations of air pollutants. In addition, we used conditional logistic regression and the distributed lag nonlinear model to calculate the prevalence ratios of CKD and the 95% confidence interval. Confounders including Framingham Risk Score (FRS), diabetes, gout, arthritis, heart disease, metabolic syndrome and vegetables consumption were adjusted in the models.
Results
Participants with a high FRS (>10%), diabetes, heart disease, gout, arthritis or metabolic syndrome had significantly increased CKD prevalence. After adjustment for confounders, PM2.5 levels were significantly increased in CKD cases in both single- and two-pollutant models (prevalence ratio 1.31–1.34). There was a positive association with CKD in the two-pollutant models for NO2. However, similar results were not observed for SO2.
Conclusions
FIS may be helpful to reduce uncertainty with better interpolation for limited monitoring stations. Meanwhile, long-term exposure to ambient PM2.5 appears to be associated with an increased prevalence of CKD, based on a FIS model.
... CKD is a multifactorial disease, with risk factors including environmental factors, body mass index (BMI), infections, auto-immune disorders, diabetes, hypertension, ageing, genetic predisposition and lifestyle (Kazancioglu, 2013;Kataria et al., 2015). An increasing number of studies have linked air pollution exposure to reduced renal function and increased risk of CKD in adults (Bowe et al., 2017(Bowe et al., , 2018Mehta et al., 2016;Lin et al., 2020aLin et al., , 2020bLi et al., 2021aLi et al., , 2021bHwang et al., 2021;Chan et al., 2018;Blum et al., 2020;Lue et al., 2013). In agreement with this, it has been reported that exposure to residential greenness or improved air quality can reduce the risk of developing CKD in adults (Liang et al., 2021a;Bo et al., 2021). ...
Background
Few studies have examined the effects of multi-pollutant air pollution on renal health, especially in children and adolescents. This study investigated the association between long-term ambient air pollution exposure and renal health in Asian children and adolescents.
Methods
This study included 10,942 children and adolescents from Taiwan and Hong Kong between 2000 and 2017. PM2.5, NO2 and O3 concentrations were estimated using satellite-based spatiotemporal regression models. Two-year average concentrations, those of the year of visit and the preceding year, were used. Linear mixed models were used to examine the association between air pollution and yearly changes in estimated glomerular filtration rate (eGFR). Cox regression models with time-dependent covariates were used to examine the association between air pollution and the development of chronic kidney disease (CKD).
Results
Median age of the participants was 19 years (range: 2–25). The overall average concentration of PM2.5, NO2 and O3 was 26.7 μg/m³, 44.1 μg/m³ and 51.1 μg/m³, respectively. The mean yearly change in eGFR was 0.37 μL/min/1.73 m² and the incidence rate of CKD was 6.8 per 1,000 person-years. In single-pollutant models, each 10 μg/m³ increase in PM2.5 was associated with a 0.45 μL/min/1.73 m² [95% confidence interval (CI): 0.28–0.63] reduction in the yearly increase in eGFR and 53% [hazard ratio (HR): 1.53 (95%CI: 1.07–2.2)] greater risk of incident CKD. Each 10 μg/m³ increase in NO2 was associated with a 7% [HR (95%CI): 1.07 (1.00–1.15)] higher risk of incident CKD, while an equivalent increase in O3 was associated with a 19% [HR (95%CI): 0.81 (0.67–0.98)] lower risk.
Conclusions
Long-term exposure to ambient PM2.5 and NO2 was associated with a slower growth of eGFR and a higher risk of incident CKD in children and adolescents. Our findings suggest that air pollution control in early life is imperative to improve lifelong renal health and alleviate the CKD burden.
... In vitro and in vivo studies have shown that traffic-related diesel PM exposure can induce nephrotoxicity by promoting oxidative stress, inflammation, and DNA damage (13,14). Residential proximity to major roadways and increased levels of PM 2.5 in a cohort of patients with acute ischemic stroke were associated with reduced estimated glomerular filtration rate (eGFR) (15). In the Veterans Administrative Normative Aging Study cohort, long-term environmental exposure to higher concentrations of ambient fine PM in elderly patients with mean eGFR of 76.5 ml/min/1.73 ...
Limited literature has explored the effect of air pollutants on chronic kidney disease (CKD) progression, especially for patients with pre-end-stage renal disease (pre-ESRD). In this study, we reported the linear and nonlinear relationships of air pollutants of particles with diameter <2.5 μm (PM2.5) and nitrogen dioxide (NO2) with estimated glomerular filtration rate (eGFR) deterioration after adjusting for smoking status and other traditional clinical factors. This study adopted a retrospective cohort of patients with stage 3b to stage 5 CKD (N = 11,479) from Taichung Veterans General Hospital during January 2006 to December 2020. The eGFR deterioration was defined as a decline in eGFR > 5 ml/min/1.73 m²/year. Hybrid kriging/land-use regression models were used to estimate the individual exposure levels of PM2.5 and NO2. The relationships of air pollutants with eGFR deterioration were evaluated using Cox proportional hazard models. After adjusting for smoking status, baseline eGFR stages, and other traditional clinical factors, the risk of eGFR deterioration was found to increase with increasing PM2.5 and NO2 level (p < 0.0001 and p = 0.041, respectively), especially for those exposed to PM2.5 ≥ 31.44 μg/m³ or NO2 ≥ 15.00 ppb. Similar results were also found in the two-pollutant models. Nonlinear dose–response relationships of eGFR deterioration were observed for concentrations of 26.11 μg/m³ for PM2.5 and 15.06 ppb for NO2. In conclusion, linear and nonlinear associations between PM2.5 and NO2 levels and the incidence risk of eGFR deterioration were observed in patients with pre-ESRD.
... Была выявлена связь между близостью жилой застройки к транспортным потокам и маркером клеточного иммунитета in vitro [18]. Исследовательское подразделение сердечно-сосудистой эпидемиологии Массачусетса США выявило, что проживание вблизи основных дорог способствует снижению функции почек и повышению риска сердечнососудистых заболеваний [19]. ...
Environmental management and planning of the urban environment, the inclusion of natural landscapes in it is becoming increasingly important today. The paper discusses the latest researches in printed Russian and foreign publications that study the impact of roads and roadside landscaping on the quality of the urban environment and the life of citizens. The dependence of the influence of urban greening on temperature, runoff, heat flows, carbon dioxide, the content of solid particles and gas pollution is shown. The analysis of studies in which environmental recommendations are given to reduce these impacts is carried out. Roads as a dangerous object of urbanized environment should be surrounded by a buffer green zone. The importance of studying the location of the main streets and identifying landscaping around them in urban centers is indicated. The paper contains an assessment of the environmental parameters of roadside zones, depending on the level of their landscaping and the remoteness of residential development from the roadway, in large cities of the Orenburg Region. General and specific recommendations on environmental optimization of spaces have been compiled, allowing to reduce the environmental burden on the roadside environment through effective planning of green infrastructure, which will provide a basis for improving the health of the population and their quality of life.
... Another possible explanation is that PM 2.5 exposure could impact the CVD case fatality rate, which could be assessed in future studies instead of first CVD event since followup to take all incident CVD events into account and to further understand PM's impact on cardiovascular health among this population. In addition, evidence is emerging that elevated levels of fine particulate matter may contribute to incident chronic kidney disease, and its progression to severe kidney function impairment that requires maintenance dialysis treatment [31][32][33]. Together with previously published studies, our findings support the conclusion that there is an elevated health hazard associated with particulate matter exposure among dialysis patients. Furthermore, the daily ZIP code-level PM 2.5 for the majority (Q3 of 10.6 µg/m 3 ) of the included person-days in this analysis were below the current NAAQS regulatory standard of 35 µg/m 3 (24-h, 98 th percentile). ...
Background
Ambient PM2.5 is a ubiquitous air pollutant with demonstrated adverse health impacts in population. Hemodialysis patients are a highly vulnerable population and may be particularly susceptible to the effects of PM2.5 exposure. This study examines associations between short-term PM2.5 exposure and cardiovascular disease (CVD) and mortality among patients receiving maintenance in-center hemodialysis.
Methods
Using the United State Renal Data System (USRDS) registry, we enumerated a cohort of all US adult kidney failure patients who initiated in-center hemodialysis between 1/1/2011 and 12/31/2016. Daily ambient PM2.5 exposure estimates were assigned to cohort members based on the ZIP code of the dialysis clinic. CVD incidence and mortality were ascertained through 2016 based on USRDS records. Discrete time hazards regression was used to estimate the association between lagged PM2.5 exposure and CVD incidence, CVD-specific mortality, and all-cause mortality 1 t adjusting for temperature, humidity, day of the week, season, age at baseline, race, employment status, and geographic region. Effect measure modification was assessed for age, sex, race, and comorbidities.
Results
Among 314,079 hemodialysis patients, a 10 µg/m³ increase in the average lag 0–1 daily PM2.5 exposure was associated with CVD incidence (HR: 1.03 (95% CI: 1.02, 1.04)), CVD mortality (1.05 (95% CI: 1.03, 1.08)), and all-cause mortality (1.04 (95% CI: 1.03, 1.06)). The association was larger for people who initiated dialysis at an older age, while minimal evidence of effect modification was observed across levels of sex, race, or baseline comorbidities.
Conclusions
Short-term ambient PM2.5 exposure was positively associated with incident CVD events and mortality among patients receiving in-center hemodialysis. Older patients appeared to be more susceptible to PM2.5-associated CVD events than younger hemodialysis patients.
... Previous reviews reported that exposure to PM 2.5 may increase oxidative stress and inflammation , and these responses were found to be related with renal dysfunction in some populations (Yilmaz et al., 2006;Upadhyay et al., 2011;Correia-Costa et al., 2016). Since kidney is a highly vascularized organ and is susceptible to vascular dysfunction (Lue et al., 2013). Increased states of vasoconstriction and blood coagulation could decrease renal blood flow, further weakening the filtration function of the kidney. ...
Exposure to fine particulate matter (PM2.5) has been reported to increase the risks of chronic kidney disease. However, limited research has assessed the effect of PM2.5 and its constituents on renal function, and the underlying mechanism has not been well characterized. We aimed to evaluate the association of PM2.5 and its constituents with kidney indicators and to explore the roles of systematic oxidative stress and inflammation in the association. We conducted a longitudinal panel study among 35 healthy adults before-, intra- and after-the 2019 Wuhan Military World Games. We repeatedly measured 6 renal function parameters and 5 circulating biomarkers of oxidative stress and inflammation at 6 rounds of follow-ups. We monitored hourly personal PM2.5 concentrations with 3 consecutive days and measured 10 metals (metalloids) and 16 polycyclic aromatic hydrocarbons (PAHs) components. The linear mixed-effect models were applied to exam the association between PM2.5 and renal function parameters, and the mediation analysis was performed to explore potential bio-pathways. PM2.5 concentrations across Wuhan showed a slight decrease during the Military Games. We observed significant associations between elevated blood urea nitrogen (BUN) levels and PM2.5 and its several metals and PAHs components. For an interquartile range (IQR) increase of PM2.5, BUN increased 0.42 mmol/L (95% CI: 0.14 to 0.69). On average, an IQR higher of lead (Pb), cadmium (Cd), arsenic (As), selenium (Se), thallium (Tl) and Indeno (1,2,3-cd) pyrene (IPY) were associated with 0.90, 0.65, 0.29, 0.27, 0.26 and 0.90 mmol/L increment of BUN, respectively. Moreover, superoxide dismutase was positively associated with PM2.5 and mediated 18.24% association. Our research indicated that exposure to PM2.5 might affect renal function by activating oxidative stress pathways, in which the constituents of Pb, Cd, As, Se, Tl and IPY might contribute to the associations.
... There have been few studies on the relationship between noise and renal function. An epidemiological study of 1103 patients from the Boston area in the United States who had ischemic stroke showed lower eGFR as they live closer to a major roadway 15 . Moreover, in 217 patients with cardiovascular heart disease, increased exposure to day-evening-night noise levels (L den ) resulted in a decrease in eGFR among men who experienced ischemic heart disease or stroke and who were exposed to lower air pollution 16 . ...
Exposure to occupational and environmental noise is closely linked to various auditory system diseases. Few studies have focused on the effect of noise exposure on the extra auditory system, especially the urinary system. We analyzed 17,154 participants aged 40–79 years from the Korea National Health and Nutrition Examination Survey between 2013 and 2018. A self-reported questionnaire was used to assess occupational or environmental noise exposure. Logistic regression was used to determine the differences in the prevalence of chronic kidney disease (CKD) based on noise exposure characteristics. For participants with noise exposure, linear regression was performed to determine relationship of the noise exposure period and estimated glomerular filtration rate (eGFR). In the noise exposure group, a higher CKD prevalence was associated with females who experienced long-term occupational noise (≥ 240 months) (adjusted OR 2.72, 95% CI 1.11–6.66). An increase of one month of occupational noise exposure was associated with a 0.0106 mL/min/1.73 m ² decrease in eGFR in females aged < 60 years. Overall, noise exposure may be a risk factor for reduced renal function, especially long-term occupational noise exposure. More precise studies should determine (1) the relationship between noise and renal function and (2) the underlying mechanisms.
... P ¼ 0.007). The decrease of renal function in patients living 50 m away from the main road is equal to the decrease of natural physiological renal function with the increase of age by 4 years (Lue et al. 2013). ...
The impact of ambient particulate matter (PM) on public health has become a great global concern, which is especially prominent in developing countries. For health purposes, PM is typically defined by size, with the smaller particles having more health impacts. Particles with a diameter <2.5 μm are called PM2.5. Initial research studies have focused on the impact of PM2.5 on respiratory and cardiovascular diseases; nevertheless, an increasing number of data suggested that PM2.5 may affect every organ system in the human body, and the kidney is of no exception. The kidney is vulnerable to particulate matter because most environmental toxins are concentrated by the kidney during filtration. According to the high morbidity and mortality related to chronic kidney disease, it is necessary to determine the effect of PM2.5 on kidney disease and its mechanism that needs to be identified. To understand the current status of PM2.5 in the atmosphere and their potential harmful kidney effects in different regions of the world this review article was prepared based on peer-reviewed scientific papers, scientific reports, and database from government organizations published after the year 1998. In this review, we focus on the worldwide epidemiological evidence linking PM2.5 with chronic kidney disease and the effect of PM2.5 on the chronic kidney disease (CKD) progression. At the same time, we also discuss the possible mechanisms of PM2.5 exposure leading to kidney damage, in order to emphasize the contribution of PM2.5 to kidney damage. A global database on PM2.5 and kidney disease should be developed to provide new ideas for the prevention and treatment of kidney disease.
... Similar finding has been described in a cohort of US veterans (Bowe et al. 2017). A cohort aimed at acute ischemic stroke patients showed that people living near a major roadway had a lower EGFR due to higher levels of air pollutants (Lue et al. 2013). Ambient particulate exposure was correlated with elevated circulating C-reactive protein (CRP) levels, pointing to an activated systemic inflammatory state (Liu et al. 2019). ...
Chronic kidney disease (CKD), a global disease burden related to high rates of incidence and mortality, manifests as progressive and irretrievable nephron loss and decreased kidney regeneration capacity. Emerging studies have suggested that exposure to air pollution is closely relevant to increased risk of CKD, CKD progression and end-stage kidney disease (ESKD). Inhaled airborne particles may cause vascular injury, intraglomerular hypertension, or glomerulosclerosis through non-hemodynamic and hemodynamic factors with multiple complex interactions. The mechanisms linking air pollutants exposure to CKD include elevated blood pressure, worsening oxidative stress and inflammatory response, DNA damage and abnormal metabolic changes to aggravate kidney damage. In the present review, we will discuss the epidemiologic observations linking air pollutants exposure to the incidence and progression of CKD. Then, we elaborate the potential roles of several air pollutants including particulate matter and gaseous co-pollutants, environmental tobacco smoke, and gaseous heavy metals in its pathogenesis. Finally, this review outlines the latent effect of air pollution in ESKD patients undergoing dialysis or renal transplant, kidney cancer and other kidney diseases. The information obtained may be beneficial for further elucidating the pathogenesis of CKD and making proper preventive strategies for this disease.
... Patients living at a distance of 50 m vs. 1 km had a 3.9 mL/min/1.73 m 2 lower eGFR (P = 0.007) 5 . Among 21,656 residents of Taipei (2007)(2008)(2009) 7 , eGFR and the prevalence of CKD (eGFR < 60 mL/min/1.73 ...
From 1990 until 2017, global air-pollution related mortality increased by 40%. Few studies addressed the renal responses to ultrafine particulate [≤ 2.5 µm (PM2.5)], including black carbon (BC), which penetrate into the blood stream. In a Flemish population study, glomerular filtration estimated from serum creatinine (eGFR) and the urinary albumin-to-creatinine ratio were measured in 2005–2009 in 820 participants (women, 50.7%; age, 51.1 years) with follow-up of 523 after 4.7 years (median). Serum creatinine, eGFR, chronic kidney disease (eGFR < 60 mL/min/1.73 m²) and microalbuminuria (> 3.5/> 2.5 mg per mmol creatinine in women/men) were correlated in individual participants via their residential address with PM2.5 [median 13.1 (range 0.3–2.9) μg/m³] and BC [1.1 (0.3–18) μg/m³], using mixed models accounting for address clusters. Cross-sectional and longitudinally, no renal outcome was associated with PM2.5 or BC in models adjusted for sex and baseline or time varying covariables, including age, blood pressure, heart rate, body mass index, plasma glucose, the total-to-HDL serum cholesterol ratio, alcohol intake, smoking, physical activity, socioeconomic class, and antihypertensive treatment. The subject-level geocorrelations of eGFR change with to BC and PM2.5 were 0.13 and 0.02, respectively (P ≥ 0.68). In conclusion, in a population with moderate exposure, renal function was unrelated to ultrafine particulate.
... Comparing patients living 0.05 km vs. 1 km from a major roadway, the first group was associated with a 3.9 mL/min/1.73m 2 lower eGFR (95%CI: 1.0-6.7; P = 0.007) than the latter one 27 . In a population-based cohort of veterans in the USA, a 10-µg/m 3 increase in PM 2.5 concentration was associated with increased risk of CKD (Hazard ratio = 1.21; 95%CI 1.14-1.29) ...
Air pollution contributes to the premature death of approximately 428,000 citizens of Europe every year. The adverse effects of air pollution can be observed in respiratory, circulatory systems but also in renal function. We decide to investigate the hypothesis indicating that we can observe not only long-but also short-term impact of air pollution on kidney function. We used linear, log-linear, and logistic regression models to assess the association between renal function and NO 2 , SO 2 , and PMs. Results are reported as beta (β) coefficients and odds ratios (OR) for an increase in interquartile range (IQR) concentration. 3554 patients (median age 66, men 53.2%) were included into final analysis. Chronic kidney disease (CKD) was diagnosed in 21.5%. The odds of CKD increased with increase in annual concentration of PM 2.5 (OR for IQR increase = 1.07; 95% CI 1.01-1.15, P = 0.037) and NO 2 (OR for IQR increase = 1.05; 95% CI 1.01-1.10, P = 0.047). The IQR increase in weekly PM 2.5 concentration was associated with 2% reduction in expected eGFR (β = 0.02, 95% CI − 0.03; − 0.01). Medium-and short-term exposure to elevated air pollution levels was associated with a decrease in eGFR and development CKD. The main pollutants affecting the kidneys were PM 2.5 and NO 2.
... Shih-Ho Lue et al. [28] observed a lower estimated GFR in patients living closer to a major roadway than in patients living farther away. The renal function decreased almost exponentially with increasing residential proximity to the major roadway. ...
Background:
Chronic mental stress is recognized as a modifiable risk factor for cardiovascular disease. The aim of this study was to demonstrate that noise annoyance-induced stress is associated with changes in renal hemodynamics.
Methods:
Renal hemodynamic parameters were measured using steady-state input clearance with infusion of para-aminohippuric acid and inulin in individuals with normal, high normal, and elevated blood pressure. All individuals ranked subjective annoyance due to noise in everyday life on a 7-grade Likert scale. The median of all rankings was used as a cutoff point to divide the group into noise-annoyed and non-noise-annoyed individuals. Different renal hemodynamic parameters were calculated based on the Gomez equation.
Results:
Noise-annoyed individuals (n = 58) showed lower renal plasma flow (599 ± 106 vs. 663 ± 124 mL/min, p = 0.009), lower renal blood flow (1,068 ± 203 vs. 1,172 ± 225 mL/min, p = 0.047), higher filtration fraction (22.7 ± 3.3 vs. 21.3 ± 3.0, p = 0.012), higher renal vascular resistance (88.9 ± 25.6 vs. 75.8 ± 22.9 mm Hg/[mL/min], p = 0.002), and higher resistance of afferent arteriole (2,439.5 ± 1,253.4 vs. 1,849.9 ± 1,242.0 dyn s-1 cm-5, p = 0.001) compared to non-noise-annoyed individuals (n = 55). There was no difference in measured glomerular filtration rate (133 ± 11.8 vs. 138 ± 15 mL/min, p = 0.181), resistance of efferent arteriole (2,419.4 ± 472.2 vs. 2,245.8 ± 370.3 dyn s-1 cm-5, p = 0.060), and intraglomerular pressure (64.0 ± 3.1 vs. 64.6 ± 3.5 mm Hg, p = 0.298) between the groups. After adjusting for age, renal plasma flow, renal blood flow, and renal vascular resistance remained significantly different between the groups, with a trend in increased afferent arteriolar resistance and filtration fraction.
Conclusion:
In this study, noise annoyance was associated with reduced renal perfusion attributed to increased renal vascular resistance predominantly at the afferent site. Long-term consequences of this renal hemodynamic pattern due to noise annoyance need to be investigated.
... In the USA, elevated levels of fine particulate matter are associated with incident CKD, decline in estimated glomerular filtration rate, and progression to kidney failure [13,14]. In fact, proximity to major roads and increased levels of PM 2.5 lead to reduced estimated glomerular filtration rate [15]. ...
Background:
Fine particulate matter (particulate matter with diameter <2.5 µm [PM2.5]) is associated with CKD progression and may impact the health of patients living with kidney failure. While older (aged ≥65 years) adults are most vulnerable to the impact of PM2.5, it is unclear whether older patients on dialysis are at elevated risk of mortality when exposed to fine particulate matter.
Methods:
Older adults initiating dialysis (2010-2016) were identified from US Renal Data System (USRDS). PM2.5 concentrations were obtained from NASA's Socioeconomic Data and Application Center (SEDAC) Global Annual PM2.5 Grids. We investigated the association between PM2.5 and all-cause mortality using Cox proportional hazard models with linear splines [knot at the current Environmental Protection Agency (EPA) National Ambient Air Quality Standard for PM2.5 of 12 μg/m3] and robust variance.
Results:
For older dialysis patients who resided in areas with high PM2.5, a 10 μg/m3 increase in PM2.5 was associated with 1.16-fold (95% CI: 1.08-1.25) increased risk of mortality; furthermore, those who were female (aHR = 1.26, 95% CI: 1.13-1.42), Black (aHR = 1.31, 95% CI: 1.09-1.59), or had diabetes as a primary cause of kidney failure (aHR = 1.25, 95% CI: 1.13-1.38) were most vulnerable to high PM2.5. While the mortality risk associated with PM2.5 was stronger at higher levels (aHR = 1.19, 95% CI: 1.08-1.32), at lower levels (≤12 μg/m3), PM2.5 was significantly associated with mortality risk (aHR = 1.04, 95% CI: 1.00-1.07) among patients aged ≥75 years (Pslope difference = 0.006).
Conclusions:
Older adults initiating dialysis who resided in ZIP codes with PM2.5 levels >12 μg/m3 are at increased risk of mortality. Those aged >75 were at elevated risk even at levels below the EPA Standard for PM2.5.
... m2 lower eGFR (95%CI: 1.0-6.7; p=0.007) than the latter one [28]. In a population-based cohort of veterans in the USA, a 10-µg/m 3 increase in PM 2.5 concentration was associated with increased risk of CKD (Hazard ratio=1.21; ...
Introduction: Air pollution contributes to the premature death of approximately 428,000 citizens of Europe every year. The adverse effects of air pollution can be observed not only in respiratory, circulatory, and nervous systems but also in renal function.
Aim: Our goal was to investigate the hypothesis indicating that we can observe the long-term and also short-term impact of air pollution on kidney function.
Methods: We reviewed medical notes of patients hospitalized at Medical University of Bialystok, Poland between 2007-2016. We used linear, log-linear, and logistic regression models to assess the association between renal function and NO2, SO2, and PMs. Results are reported as beta (β) coefficients and odds ratios (OR) for an increase in interquartile range (IQR) concentration with 95% confidence intervals (95%CI).
Results: 3,554 patients were included into the final analysis. The median age was 66 (IQR 15) and men were in the majority (53.2%, N=1891). Chronic kidney disease (CKD) was diagnosed in 21.5% (N=764). The long-term increase in annual average concertation of PM2.5 (OR for IQR increase=1.07; 95% CI 1.01 – 1.15, P=0.037) and NO2 (OR for IQR increase=1.05;95% CI 1.01 – 1.10, P=0.047) resulted in an increased number of patients with CKD. In short-term observation the IQR increase in weekly PM2.5 concentration was associated with a 2% reduction in eGFR (OR=0.98, 95%CI 0.97 – 0.99, P=0.03)
Conclusions: The effects of air pollution on renal function were observed. Long- and short–term exposure to elevated air pollution levels was associated with a decrease in eGFR. The main pollutant affecting the kidneys was PM2.5.
... Recently, epidemiological evidence has also reported the association of a decline of glomerular filtration rate (GFR) with PM 2.5 exposure near a principal roadway (Lue et al., 2013). An association between the reduction of GFR with the exposure to PM 2.5 has recently been reported in a group of elderly men from Boston, Massachusetts (Mehta et al., 2016). ...
PM2.5 exposure is associated with a glomerular filtration rate (GFR) reduction, and renal tissue damage. The goal of this study was demonstrate the acute effect of PM2.5 on the kidney. Male rats were acutely exposed to PM2.5 or filtered air. Blood pressure was mesure and early kidney biomarkers were evaluated in serum and urine samples, and also IL-1β, IL-6 and TNFα were determined. Oxidative biomarkers, angiotensin/bradykinin-related proteins, KIM-1, IL-6 and histology were determined. Blood pressure, GFR, and early kidney damage biomarkers increase together with oxidative biomarkers and angiotensin/bradykinin endocrine-related proteins increased after exposure to PM2.5. Urinary IL-6 increased after exposure to PM2.5, whereas in kidney cortex decreased. Histological changes were observed and accompanied by the induction of KIM-1. Acute exposure to PM2.5 not decline kidney function. However, it can induce early kidney damage biomarkers, oxidative stress, inflammation and angiotensin mediators, which perhabs culminates in a lose of renal function.
... The kidney is a vascularized organ, susceptible to vascular dysfunction. 30 Experimental evidence has shown that exposure to diesel exhaust particles, which are a major source for urban ambient PM 2.5 , exacerbated vascular damage in rats 31 and facilitated progression to tubular damage. 32 In addition, diesel exhaust particles also induced nephrotoxicity in vitro and in vivo through autophagy, endoplasmic-reticulum stress, and apoptosis in kidney tissues. ...
Background:
Fine particulate matter (PM2.5) is an important environmental risk factor for cardiopulmonary diseases. However, the association between PM2.5 and risk of CKD remains under-recognized, especially in regions with high levels of PM2.5, such as China.
Methods:
To explore the association between long-term exposure to ambient PM2.5 and CKD prevalence in China, we used data from the China National Survey of CKD, which included a representative sample of 47,204 adults. We estimated annual exposure to PM2.5 before the survey date at each participant's address, using a validated, satellite-based, spatiotemporal model with a 10 km×10 km resolution. Participants with eGFR <60 ml/min per 1.73 m2 or albuminuria were defined as having CKD. We used a logistic regression model to estimate the association and analyzed the influence of potential modifiers.
Results:
The 2-year mean PM2.5 concentration was 57.4 μg/m3, with a range from 31.3 to 87.5 μg/m3. An increase of 10 μg/m3 in PM2.5 was positively associated with CKD prevalence (odds ratio [OR], 1.28; 95% confidence interval [CI], 1.22 to 1.35) and albuminuria (OR, 1.39; 95% CI, 1.32 to 1.47). Effect modification indicated these associations were significantly stronger in urban areas compared with rural areas, in males compared with females, in participants aged <65 years compared with participants aged ≥65 years, and in participants without comorbid diseases compared with those with comorbidities.
Conclusions:
These findings regarding the relationship between long-term exposure to high ambient PM2.5 levels and CKD in the general Chinese population provide important evidence for policy makers and public health practices to reduce the CKD risk posed by this pollutant.
... One of the simplest types of exposure assessment models for air pollution is a proximity model that assesses exposure based on proximity to an emissions source. The natural logarithm of road proximity is frequently used as a surrogate for traffic-related air pollution in epidemiological studies (Henry, Anthopolos, and Maxson 2013;Lue et al. 2013;Wilker et al. 2016). A previous study from our group showed indoor concentrations of various traffic-related elements were related to log distance to road (Huang et al. 2018). ...
Traffic-related air pollution is associated with various adverse health effects. In the absence of more complicated exposure assessment techniques, many environmental health studies have used natural logarithm of distance to road as a proxy for traffic-related exposures. However, research validating this proxy and further explaining the spatial patterns and elemental composition of traffic-related particulate matter air pollution remains limited. In this study we collected air samples using a mobile particle concentrator that allowed for high sample loading from major roadways in the Greater Boston Area. We found that concentrations of Cl, Ti, V, Cr, Mn, Fe, Co, Cu, Zn, Sr, Zr, Sn, Ba, and Pb were significantly associated with natural logarithm of distance to road in coarse particulate matter, and total fine particulate mass concentration, Al, Ca, Ti, Cr, Mn, Fe, Cu, and Zn were significantly associated with natural logarithm of distance to road in fine particulate matter. Road type (A1 or A2 (primary roads or highways) versus A3 (secondary and connecting roads)) was not a significant predictor of any traffic-related elements in particulate matter air pollution. Our results help identify traffic-related elements in particulate matter air pollution and support the use of logarithm of distance to road as a proxy for traffic-related particulate matter air pollution exposure assessment in epidemiological studies.
... Despite global rising prevalence of ESRD, limited studies have reported the effect of long-term exposure to PM 2.5 on the incidence of ESRD in general populations. In a cross-sectional study of 1103 patients with diagnosed ischemic stroke in the U.S., Lue et al. have shown that residing nearby major roads is negatively associated with the estimated glomerular filtration rate (eGFR) (Lue et al., 2013). In another crosssectional study of an elderly population in the U.S., Bragg-Gresham et al. have observed a positive association between county-level PM 2.5 and diagnosed CKD (Bragg-Gresham et al., 2018). ...
The rising prevalence and incidence of end-stage renal disease (ESRD) have been noted around the world. However, no study has been conducted to examine the effect of surrounding environment on incidence of ESRD. This study assessed the associations of exposure to PM2.5 level and surrounding green spaces, separately, with incidence of ESRD in Taiwan. Demographic and clinical data used in this study was retrieved from the National Health Insurance Research Database from 2003 to 2012.
PM2.5 data collected from the Environmental Protection Administration of Taiwan and a hybrid land-use regression model was used to approximate long-term exposure to PM2.5. Percentage of exposure to surrounding green spaces was used to determine individual exposure level. Cox proportional hazards models with a generalized estimating equation were applied to investigate the effect of surrounding environment on incidence of ESRD.
The results showed significant positive association between exposure to PM2.5 level and incidence of ESRD; but inverse association between exposure to surrounding green spaces and incidence of ESRD (adjusted hazard ratio (AHR) = 1.08, 95% CI: 1.00–1.15 for exposure to PM2.5 level; AHR = 0.90, 95%CI: 0.84–0.98 for surrounding green spaces). Together, the findings from this study have added suggestive evidence on the adverse effect of exposure to PM2.5 level and the beneficial effect of exposure to surrounding green spaces on the incidence of ESRD in a general population in Taiwan.
... Another study on 24,407 adults in Korea reported that exposure to airborne PM 10 and nitrogen dioxide (NO 2 ) are significantly associated with a decrease in eGFR levels (Glazer et al., 2018). A study by Leo et al., on 1103 patients admitted for brain stroke found that the level of eGFR in patients who lived less than 50 m away from a major road was less than those whose residence was more than 1000 m away from a major road (Lue et al., 2013). A longitudinal study on the 669 older men showed that exposure to PM 2.5 had a negative association on renal function characterized as serum level of Cr and calculated eGFR (Mehta et al., 2016a). ...
Exposure to air pollution has been associated with different harmful effects and exposure to greenspace has been related to improved human health. However, the available evidence on the impact of these exposures on renal function is still scarce. The aim of this study was to determine the relationship between exposure to ambient levels of PM1, PM2.5, PM10 and indicators of exposure to traffic as well as greenspace during pregnancy and fetal renal function based on the umbilical cord blood. This study was based on 150 pregnant women residing in Sabzevar, Iran (2018). Multiple linear regression models were developed to estimate the association of glomerular filtration rate (GFR), creatinine (Cr) and blood urea nitrogen (BUN) with exposure to air pollution, traffic, and greenspace (one at a time) controlled for relevant covariates. There was an inverse significant association between exposure to PM1, PM2.5, PM10 and total street length in a 100 m buffer around the home and eGFR. Increase in distance to major road and residential surrounding greenness (100 m buffer) was associated with increase in eGFR. We observed a significant direct association between exposure to PMs as well as street length in 100 m buffer and serum level of Cr. There was also an inverse association between distance to major road and NDVI in 100 m buffer and Cr. The associations for blood urea nitrogen (BUN) were not statistically significant. Our results suggest that exposure to air pollution during pregnancy could have negative impact and exposure to greenspace could have positive impact on renal function of fetal.
... In a cohort study of patients with stroke, those living within 50 m of a main roadway had a 3.9 ml/min/1.73 m 2 lower eGFR than those who lived > 1000 m from a major roadway [18]. Several biological mechanisms have been proposed to explain this negative association between air pollutant concentrations and impaired kidney function. ...
This study aimed to evaluate the associations between ambient air pollutants, obesity, and kidney function.
We enrolled 3345 people who had undergone health checkups at Seoul National University Hospital. We recorded the annual average concentrations of ambient air pollutants, including particulate matter with an aerodynamic diameter of ≤10 μm (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), and carbon monoxide (CO), in each subject’s residential area. Various obesity traits, such as body mass index, waist circumference, and visceral and subcutaneous adipose tissue areas, were measured by quantified computerized tomography (CT), and kidney function was assessed in relation to estimated glomerular filtration rate as an indicator of kidney function.
High PM10, NO2, SO2, and CO concentrations were significantly associated with decreased kidney function (β = −2.39 and standard error = 0.32, −1.00 and 0.31, −1.23 and 0.28, and −1.32 and 0.29, respectively), and with the prevalence of chronic kidney disease (CKD). The association between air pollutant concentrations and decreased kidney function, including CKD, was stronger among those with high abdominal adiposity, as defined by CT measurement. For example, the association between increased concentrations of air pollutants and the prevalence of CKD was stronger in the group with greater visceral adiposity than in the group with less visceral adiposity (aORs = 1.29 vs 1.16 for PM10, 1.42 vs 1.21 for SO2, and 1.27 vs 1.11 for CO).
Long-term exposure to higher concentrations of air pollutants was unfavorably associated with kidney function and CKD prevalence, especially in people with abdominal obesity. This may indicate a high susceptibility to air pollutants in obese people.
Objective
We aimed to explore the effect of particulate matter (PM) exposure on renal function in people living with HIV/AIDS (PWHA).
Methods
A total of 37,739 repeated measurements were conducted on eGFR levels, serum creatinine (Scr), and the triglyceride-glucose (TyG) index in 6,958 PWHAs. The relationship between 1–28 day moving averages of PM concentrations with Scr and eGFR was assessed using linear mixed-effects models. Modified Poisson regression models were employed to assess the associations of cumulative PM exposure with the incidence of chronic kidney disease (CKD). Mediation analyses were used to examine the role of TyG index.
Results
Short-term exposure to PM was related to reduced renal function. The strongest associations between exposure to PM 1 , PM 2.5 , and PM 10 and percent changes in eGFR were observed at 7-day moving average exposure windows, with a respective decrease of 0.697% (−1.008%, −0.386%), 0.429% (−0.637%, −0.220%), and 0.373% (−0.581%, −0.164%) per IQR increment. Long-term exposure to PM 1 , PM 2.5 , and PM 10 was positively linked with the incidence of CKD, with each IQR increment corresponding to fully adjusted RRs (95% CIs) of 1.631 (1.446, 1.839), 1.599 (1.431, 1.787), and 1.903 (1.665, 2.175), respectively. TyG index mediated 8.87%, 8.88%, and 7.58% of the relationship between cumulative exposure to PM 1 , PM 2.5 , and PM 10 and increased risk of CKD, respectively.
Conclusion
Exposure to PM among PWHAs is linked to reduced renal function, potentially contributing to increased CKD incidence, where the TyG index might serve as a partial mediator.
Chronic kidney disease (CKD) is characterized by kidney dysfunction or proteinuria lasting more than 3 months, and the number of patients is increasing worldwide. In recent years, in addition to known causes of CKD such as chronic glomerulonephritis, diabetes, and hypertension, reports have noted the risk of developing CKD due to global environmental changes, which have not been mentioned in previous Japanese epidemiological studies. It is estimated that air pollution may be related to 6.4 million deaths annually worldwide. Typical air pollutants include particulate matter (PM), sulfur dioxide, nitrogen dioxide, carbon monoxide, and ozone. Cardiovascular disease and CKD are linked and share common mechanisms of onset and disease progression. Epidemiological studies have revealed that some cardiovascular diseases are caused by air pollution, such as PM2.5. However, studies on the relationship between air pollution and CKD have been scarce, and only in the 2020s did the evidence become more comprehensive in several countries. Nevertheless, there is still no evidence on this relationship from Japan. Analysis of ozone in particular, the only pollutant whose concentration continues to rise, warrants special attention, as the results of analyses in other countries indicate that it may be a risk factor for CKD.
Background:
Ambient air pollution has become 1 of the most important public health issues worldwide. In particular, particulate matter with an aerodynamic diameter <2.5 μm (PM2.5) is a fatal component of air pollution. We aimed to analyze whether perioperative exposure to PM2.5 is associated with the deterioration of renal function in living kidney donors.
Methods:
This study was conducted on 232 kidney donors with postoperative 2-year glomerular filtration rate (GFR). The GFR was determined by serum creatinine-based method using the Modification of Diet in Renal Disease equation and radionuclide-based method using 99mTc-DTPA renal scintigraphy. Perioperative exposure to PM2.5 was calculated using data from the AIRKOREA System. Multiple linear and logistic regression analyses were performed to estimate the associations between mean PM2.5 concentration and postoperative 2-year GFR.
Results:
Postoperative Modification of Diet in Renal Disease-estimated GFRs of kidney donors with low PM2.5 concentrations were significantly higher than those of those with high PM2.5 concentrations. A 1-μg/m3 increase in mean PM2.5 concentration was associated with decreased GFR by 0.20 mL/min/1.73 m2. In addition, a 1-μg/m3 increase in mean PM2.5 concentration was associated with an 11% increased risk of chronic kidney disease stage ≥3 at 2 years after donor nephrectomy.
Conclusion:
In patients who underwent donor nephrectomy, exposure to PM2.5 negatively affects renal function and is positively associated with the prevalence of chronic kidney disease.
Growing evidence links long-term air pollution exposure with renal function. However, little research has been conducted on the combined effects of air pollutant mixture on renal function and multiple mediation effects of metabolic risk factors. This study enrolled 8996 adults without chronic kidney disease (CKD) at baseline from the CHCN-BTH cohort study. Three-year exposure to air pollutants [particulate matter ≤ 2.5 µm (PM2.5), PM10, PM1, ozone (O3), nitrogen dioxide (NO2), sulfur dioxide (SO2) and carbon monoxide (CO)] and PM2.5 components [black carbon (BC), ammonium (NH4+), nitrate (NO3-), sulfate (SO42-) and organic matter (OM)] were assessed using well-validated machine learning methods. Linear mixed models were applied to investigate the associations between air pollutants and estimated glomerular filtration rate (eGFR). Quantile G-computation was used to assess the combined effects of pollutant mixtures. Causal mediation analysis and Bayesian mediation analysis were employed to estimate the mediation effects of metabolic risk factors. An interquartile range increases in BC (-0.256, 95 %CI: -0.331, -0.180) and OM (-0.603, 95 %CI: -0.810, -0.397) were significantly associated with eGFR decline; while O3 (1.151, 95 %CI: 0.813, 1.489), PM10 (0.721, 95 %CI: 0.309, 1.133), NH4+ (0.990, 95 %CI: 0.638, 1.342), and NO3- (0.610, 95 %CI: 0.405, 0.815) were associated with higher eGFR. The combined effect of the PM2.5 component mixture was found to be associated with lower eGFR (-1.147, 95 % CI: -1.456, -0.839), with OM contributing 72.4 % of the negative effect. Univariate mediation analyses showed that high-density lipoprotein (HDL) mediated 7.1 %, 6.9 %, and 6.1 % effects of O3, BC, and OM, respectively. However, these mediation effects were not significant in Bayesian mediation analysis. These findings suggest the effect of the PM2.5 component mixture on eGFR decline and the strong contribution of OM. Metabolic risk factors may not mediate the effects of air pollutants. Further study is warranted to clarify the potential mechanisms involved.
Chronic kidney disease (CKD) has been a global public health problem with many adverse outcomes, but data are lacking regarding the relationship between air pollutants and risk of renal progression in patients with CKD. This study was to investigate whether 1-year average exposure to ambient air pollutants -CO, NO, NO2, SO2, O3, PM2.5, and PM10-is related to renal function deterioration among patients with CKD. A total of 5301 CKD patients were included in this study between October 2008 and February 2016. To estimate each patient's exposure to ambient air pollution, we used the 24-h ambient air pollution concentration monitoring data collected one year prior to renal progression or their last renal function assessment. Renal progression was considered when estimated glomerular filtration rate (eGFR) decreased more than 25% from the baseline eGFR. Cox proportional hazard regression was performed to calculate hazard ratios (HRs). Among 5301 patients with CKD, 1813 (34.20%) developed renal progression during the 30.48 ± 14.99-month follow-up. Patients with the highest quartile exposure to CO [HR = 1.53 (95% CI: 1.24, 1.88)], NO [HR = 1.38 (95% CI: 1.11, 1.71)], NO2 [HR = 1.63 (95% CI: 1.36, 1.97)], SO2 [HR = 2.27 (95% CI: 1.83, 2.82)], PM2.5 [HR = 7.58 (95% CI: 5.97, 9.62)], and PM10 [HR = 3.68 (95% CI: 2.84, 4.78)] had a significantly higher risk of renal progression than those with the lowest quartile exposure. In the multipollutant model, the analyses yielded to similar results. These results reinforce the importance of measures to mitigate air pollution and strategies to prevent worsening of kidney function in patients with CKD. One-year high exposure to ambient CO, NO, NO2, SO2, PM2.5, and PM10 is significantly associated with deteriorated kidney function in patients with CKD among Taiwanese adults.
Background
Long-term exposure to particulate air pollutants can lead to an increase in mortality of hemodialysis patients, but evidence of mortality risk with short-term exposure to ambient particulate matter is lacking. This study aimed to estimate the association of short-term exposure to ambient particulate matter across a wide range of concentrations with hemodialysis patients mortality.
Methods
We performed a time-stratified case-crossover study to estimate the association between short-term exposures to PM2.5 and PM10 and mortality of hemodialysis patients. The study included 18,114 hemodialysis death case from 279 hospitals in 41 cities since 2013. Daily particulate matter exposures were calculated by the inverse distance–weighted model based on each case's dialysis center address. Conditional logistic regression were implemented to quantify exposure-response associations. The sensitivity analysis mainly explored the lag effect of particulate matter.
Results
During the study period, there were 18,114 case days and 61,726 control days. Of all case and control days, average PM2.5 and PM10 levels were 43.98 μg/m³ and 70.86 μg/m³, respectively. Each short-term increase of 10 μg/m³ in PM2.5 and PM10 were statistically significantly associated with a relative increase of 1.07 % (95 % confidence interval [CI]: 0.99 % - 1.15 %) and 0.89 % (95 % CI: 0.84 % - 0.94 %) in daily mortality rate of hemodialysis patients, respectively. There was no evidence of a threshold in the exposure-response relationship. The mean of daily exposure on the same day of death and one-day prior (Lag 01 Day) was the most plausible exposure time window.
Conclusions
This study confirms that short-term exposure to particulate matter leads to increased mortality in hemodialysis patients. Policy makers and public health practices have a clear and urgent opportunity to pass air quality control policies that care for hemodialysis populations and incorporate air quality into the daily medical management of hemodialysis patients.
PM2.5, a harmful air pollutant, poses a severe risk to human health, especially lungs, and has obvious damage to kidneys, inducing kidney function decline, increasing the risk of suffering from chronic kidney diseases etc. In addition, it also promotes the occurrence and development of various renal tumors. The mechanism of PM2.5‐induced renal injury may involve oxidative stress, inflammatory response and cytotoxicity. This paper elaborated the kidney injures caused by PM2.5 and the corresponding possible mechanism so as to raise awareness of air pollution and reduce the damage to human body. PM2.5, a harmful air pollutant, poses a severe risk to human health. PM2.5 promotes the progression of a variety of renal diseases. This paper elaborated the kidney injures caused by PM2.5 and the corresponding possible mechanism.
Rationale & Objective
Increasing evidence has linked ambient fine particulate matter (PM2.5) to chronic kidney disease (CKD) but their association has not been fully elucidated, especially in regions with high levels of PM2.5 pollution. This study aimed to investigate the long-term association of high PM2.5 exposure on incident kidney function in mainland China.
Study Design
Prospective cohort study.
Setting
& Participants: 72,425 participants (≥ 18 years) without CKD were recruited from 121 counties in Hunan Province, China.
Exposure
Annual mean PM2.5 concentration at the residence of each participant derived from a long-term, full-coverage, high-resolution (1×1 km²), and high-quality datasets of ground-level air pollutants in China.
Outcomes
Incident CKD during the interval between the baseline examination of each participant (2Correspondence to: 005-2017) and the end of follow-up before 2018.
Analytical Approach
Cox proportional hazards models were used to estimate the independent association of PM2.5 with incident CKD and the joint association of PM2.5 with temperature or humidity on the development of PM2.5-related CKD. Restricted cubic splines were used to model exposure-response relationships.
Results
Over a median follow-up of 3.79 years (IQR, 2.03-5.48), a total of 2,188 participants with incident CKD were identified. Greater PM2.5 was associated with incident CKD with an adjusted hazard ratio (HR) of 1.70 (95% confidence interval [CI], 1.58-1.85) per 10 μg/m³ increase in long-term exposure. Multiplicative interactions between PM2.5 and humidity or temperature on incident CKD were detected (all P-interaction < 0.001), whereas an additive interaction was only detected for humidity (relative risk due to interaction [RERI], 3.59; 95% CI, 0.97-6.21).
Limitations
Lack of information on participants’ activity patterns such as time spent outdoors.
Conclusions
Greater long-term greater ambient PM2.5 pollution is associated with incident CKD in high PM2.5 exposure environments. Ambient humidity has a potentially synergetic effect on PM2.5’s association with the development of CKD.
Many countries have dedicated to the mitigation of air pollution in the past several decades. However, evidence of beneficial effects of air quality improvement on chronic kidney disease (CKD) remains limited. We thus investigated the effects of dynamic changes (including deterioration and improvement) in air quality on the incidence of CKD in a longitudinal study in Taiwan. During 2001-2016, this study recruited a total of 163,197 Taiwanese residents who received at least two standard physical examinations. The level of fine particle matter (PM2.5) was estimated using a high-resolution (1 km2) satellite-based spatio-temporal model. We defined changes of PM2.5 concentrations (ΔPM2.5) as the difference between the two-year average measurements during follow-up and during the immediately preceding visit. The time-dependent Cox regression model was adopted to evaluate the relationships between ΔPM2.5 and the incidence of CKD after adjusting for a series of covariates. The concentrations of PM2.5 in Taiwan peaked around 2004 and began to decrease since 2005. We observed an approximate linear concentration-response relationship of ΔPM2.5 with CKD incidence. Every 5 μg/m3 decrease in the ambient concentration of PM2.5 was associated with a 25% reduced risk of CKD development [hazard ratio (HR): 0.75; 95% CI: 0.73, 0.78]. In conclusion, this study demonstrated that the improvement of PM2.5 air quality might be associated with a lower risk of CKD development. Our findings indicate that reducing air pollution may effectively prevent the development of CKD.
Exposure to particulate matter has been associated with diseases of the respiratory and cardiovascular systems. Owing to the dense vasculature of the kidney, it has also been identified as a PM2.5 target organ. A potential contributor to PM2.5-mediated damage may be the promotion of inflammation. The essential oil 2-undecanone (2-methyl nonyl ketone) is an H. cordata isolate, and it has been shown to possess diverse pharmacologic effects, including anti-inflammatory properties. In this study we explored the ability of 2-undecanone to protect against PM2.5-induced kidney inflammation and the exact mechanisms in this process. We found that PM2.5 elevated the levels of certain inflammatory cytokines in BALB/c mice and in HEK 293 cells. Supplementation with 2-undecanone attenuated this PM2.5-induced inflammatory injury. Interestingly, in HEK 293 cells, the PM2.5-associated inflammation was aggravated by the mitophagy inhibitor Medivi-1, while it was attenuated by rapamycin, indicating that the mechanism of 2-undecanone-mediated inhibition of inflammation may relate to mitophagy. Meanwhile, 2-undecanone induces mitophagy in HEK 293 cells by suppressing Akt1-mTOR signaling. These results indicate that PM2.5 can induce kidney inflammation, and mitophagy induced by 2-undecanone may play a protective role against this renal inflammation.
We used real-world exposure scenarios to evaluate the effect of six ambient air pollutant (PM2.5, PM10, NO2, SO2, CO, and O3) exposure on renal function among older adults without chronic kidney disease (CKD). We recruited 169 older adults without CKD in Beijing, China, for a longitudinal study from 2016 to 2018. The Modification of Diet in Renal Disease (MDRD) and the Chronic Kidney Disease Epidemiology Collaboration (EPI) equations were employed to derive the estimated glomerular filtration rate (eGFR). A linear mixed-effects model with random intercepts for participants was employed to determine the effects of air pollutants on renal function evaluated on the basis of eGFR and urinary albumin/creatinine ratio at different exposure windows (1-, 2-, 3-, 5-, 7-, 14-, 28-, 45-, and 60-days moving averages). An interquartile range (IQR) increase in NO2 for was associated with significant decreases of in eGFR (MDRD equation) [percentage changes: -4.49 (95% confidence interval: -8.44, -0.37), -5.51 (-10.43, -0.33), -2.26 (-4.38, -0.08), -3.71 (-6.67, -0.65), -5.44 (-9.58, -1.11), -5.50 (-10.24, -0.51), -6.15 (-10.73, -1.33), and -6.34 (-11.17, -1.25) for 1-, 2-, 5-, 7-, 14-, 28-, 45-, and 60-days moving averages, respectively] and in eGFR (EPI equation) [percentage changes: -5.04 (-7.09, -2.94), -6.25(-8.81, -3.62), -5.16(-7.34, -2.92), -5.10(-7.85, -2.28), -5.83(-8.23, -3.36), -6.04(-8.55, -3.47) for 1-, 2-, 14-, 28-, 45-, and 60-days moving averages, respectively]. In two-pollutant model, only the association of NO2 exposure with eGFR remained robust after adjustment for any other pollutant. This association was stronger for individuals with hypertension for the EPI equation or BMI < 25 kg/m² for the MDRD equation at lags 1 and 1-2. Our findings suggest that NO2 exposure is associated with eGFR reduction among older adults without CKD for short (1-, 2-days) and medium (14-, 28-, 45-, 60-days) term exposure periods; thus, NO2 exposure may contribute to renal impairment.
Ambient air pollution has been identified as one of the leading causes of global burden of disease. The relationship between ambient air pollution exposure and risk of chronic kidney disease (CKD) has stimulated increasing scientific interest in the past few years. However, evidence from human epidemiological studies is still limited and inconsistent. We performed an updated systematic review and meta-analysis to clarify the potential association comprehensively. Selected electronic databases were searched for related English language studies until March 1, 2020 with a final follow-up in December 31, 2020. Risk of bias assessment for individual studies were assessed using the OHAT (Office of Health Assessment and Translation) risk-of-bias rating tool. Confidence rating and level-of-evidence conclusions were developed for bodies of evidence for a given ambient air pollutant. Summary effect estimates were calculated using random-effects meta-analyses when three or more studies are identified for the same air pollutant–CKD combination. A total of 13 studies were finally identified in our study. The meta-analytic estimates (ORs) for risk of CKD were 1.15 (95% CI: 1.07, 1.24) for each 10 μg/m³ increase in PM2.5, 1.25 (95% CI: 1.11, 1.40) for each 10 μg/m³ increase in PM10, 1.10 (95% CI: 1.03, 1.17) for each 10 ppb increase in NO2, 1.06 (95% CI: 0.98, 1.15) for each 1 ppb increase in SO2 and 1.04 (95% CI: 1.00, 1.08) for each 0.1 ppm increase in CO, respectively. The level of evidence was appraised as moderate for four of the five tested air pollutant–CKD combinations using an adaptation of the GRADE (Grading of Recommendations Assessment, Development and Evaluation) tool. In conclusion, this study suggests that certain ambient air pollutant exposure was significantly associated with an increased risk of CKD. Given the limitations, the results of this study should be interpreted with caution, and further well-designed epidemiological studies are needed to draw a definite evidence of a causal relationship.
Background
Exposure to outdoor air pollution has been linked to lung cancer, and suspicion arose regarding bladder, kidney, and urinary tract cancer (urological cancers). However, most of evidence comes from occupational studies; therefore, little is known about the effect of exposure to air pollution on the risk of urological cancers in the general population.
Method
We systematically searched Medline, Scopus, and Web of Science for articles investigating the associations between long-term exposure to air pollution and the risk of urological cancer (incidence or mortality). We included articles using a specific air pollutant (PM10, PM2.5, …) or proxies (traffic, proximity index…). We assessed each study’s quality with the Newcastle–Ottawa scale and rated the quality of the body of evidence for each pollutant-outcome with the GRADE approach. The different study methodologies regarding exposure or outcome prevented us to perform a meta-analysis.
Results
twenty articles (four case-control, nine cohort, and seven ecologic) met our inclusion criteria and were included in this review: eighteen reported bladder, six kidney, and two urinary tract. Modeling air pollutants was the most common exposure assessment method. Most of the included studies reported positive associations between air pollution and urological cancer risk. However, only a few reached statistical significance (e.g. for bladder cancer mortality, adjusted odds-ratio of 1.13 (1.03-1.23) for an increase of 4.4 μg.m-3 of PM2.5). Most studies inadequately addressed confounding, and cohort studies had an insufficient follow-up.
Discussion
Overall, studies suggested positive (even though mostly non-significant) associations between air pollution exposure and bladder cancer mortality and kidney cancer incidence. We need more studies with better confounding control and longer follow-ups.
There is a lack of evidence regarding the association of short-term exposure to fine particulate matter (PM2.5) with renal function in children and its underlying mechanism. We included 105 children aged 4–13 years from a panel study conducted in Wuhan, China with up to 3 repeated visits across 3 seasons from October 9, 2017 to June 1, 2018. We measured personal real-time PM2.5 exposure concentration continuously for 72 h preceding each round of health examinations that included serum creatinine and cytokines. Linear mixed-effects models were performed to estimate the effects of PM2.5 on estimated glomerular filtration rate (eGFR) over various lag times, and a mediation analysis was applied for the role of cytokines in association between PM2.5 and eGFR. Results showed that personal exposure to PM2.5 was dose-responsive related to decreased eGFR within lag 2 days. The effect was the strongest at lag 0 day with estimation of −1.69% [95% confidence interval (CI): -2.27%, −1.10%] in eGFR by a 10-μg/m³ increase in PM2.5, and reached peak at lag 3 h, then declined over time. Such inverse relationships were more evident among children aged 4–6 years, or boys or those who lived proximity to major roadways <300 m. Notably, eGFR still held on to decrease even when PM2.5 was below Class II Chinese ambient air quality standard at lag 0 day. Moreover, the effect of PM2.5 on eGFR was significantly reduced in children with high and medium levels of serum chemokine ligand 27 (CCL27), but not in those with low CCL27. Furthermore, CCL27 was positively relevant to PM2.5, and mediated proportion of CCL27 ranged from 3.75% to 6.61% in relations between PM2.5 and decreased eGFR over various lag times. In summary, short-term PM2.5 exposure might be dose-responsive associated with reduced eGFR whereby a mechanism partly involving CCL27 among healthy children.
Objectives:
We investigated whether long-term ambient air pollutants (AAP) exposure was associated with estimated glomerular filtration rate (eGFR) among hospitalized patients living in urban areas of Shanghai, China.
Study design:
This was a cross-sectional observational study.
Methods:
A total of 3622 newly hospitalized inpatients were investigated from October 2014 to May 2015. The prior year's average exposure to particulate matter (PM) of each participant was estimated using the Kriging interpolation method of ArcGIS. The estimated eGFR was calculated according to the chronic kidney disease epidemiology collaboration (CKD-EPI) equation. Both generalized linear and logistic regression models were applied to assess the associations between AAP and renal function.
Results:
One-year PM10 exposure was associated with lower eGFR; each standard deviation (SD) increase in PM10 was significantly associated with the increased prevalence of CKD [adjusted odds ratio (OR) 1.11; 95% confidence interval (CI): 1.02, 1.21], and lower eGFR by -0.40 (95%CI: -0.80, -0.01) ml/min/1.73 m2. Moreover, the effect of PM10 was significantly greater in people over 65 years old.
Conclusion:
Our results supported that exposure to ambient PM10 increased the risk of CKD and negatively affected renal function among Chinese adults.
Climate change is resulting in heatwaves that are more frequent, severe, and longer lasting, which is projected to double-to-triple the heat-related mortality in Boston, MA if adequate climate change mitigation and adaptation strategies are not implemented. A case-only analysis was used to examine subject and small-area neighborhood characteristics that modified the association between hot days and mortality. Deaths of Boston, Massachusetts residents that occurred from 2000–2015 were analyzed in relation to the daily temperature and heat index during the warm season as part of the case-only analysis. The modification by small-area (census tract, CT) social, and environmental (natural and built) factors was assessed. At-home mortality on hot days was driven by both social and environmental factors, differentially across the City of Boston census tracts, with a greater proportion of low-to-no income individuals or those with limited English proficiency being more highly represented among those who died during the study period; but small-area built environment features, like street trees and enhanced energy efficiency, were able to reduce the relative odds of death within and outside the home. At temperatures below current local thresholds used for heat warnings and advisories, there was increased relative odds of death from substance abuse and assault-related altercations. Geographic weighted regression analyses were used to examine these relationships spatially within a subset of at-home deaths with high-resolution temperature and humidity data. This revealed spatially heterogeneous associations between at-home mortality and social and environmental vulnerability factors.
Background: Epidemiological evidence of the effects of long-term exposure to air pollution on the chronic processes of atherogenesis is limited.
Objective: We investigated the association of long-term exposure to traffic-related air pollution with subclinical atherosclerosis, measured by carotid intima media thickness (IMT) and ankle–brachial index (ABI).
Methods: We performed a cross-sectional analysis using data collected during the reexamination (2007–2010) of 2,780 participants in the REGICOR (Registre Gironí del Cor: the Gerona Heart Register) study, a population-based prospective cohort in Girona, Spain. Long-term exposure across residences was calculated as the last 10 years’ time-weighted average of residential nitrogen dioxide (NO2) estimates (based on a local-scale land-use regression model), traffic intensity in the nearest street, and traffic intensity in a 100 m buffer. Associations with IMT and ABI were estimated using linear regression and multinomial logistic regression, respectively, controlling for sex, age, smoking status, education, marital status, and several other potential confounders or intermediates.
Results: Exposure contrasts between the 5th and 95th percentiles for NO2 (25 µg/m3), traffic intensity in the nearest street (15,000 vehicles/day), and traffic load within 100 m (7,200,000 vehicle-m/day) were associated with differences of 0.56% (95% CI: –1.5, 2.6%), 2.32% (95% CI: 0.48, 4.17%), and 1.91% (95% CI: –0.24, 4.06) percent difference in IMT, respectively. Exposures were positively associated with an ABI of > 1.3, but not an ABI of < 0.9. Stronger associations were observed among those with a high level of education and in men ≥ 60 years of age.
Conclusions: Long-term traffic-related exposures were associated with subclinical markers of atherosclerosis. Prospective studies are needed to confirm associations and further examine differences among population subgroups.
As part of a program of study to assess the exposure risks related to particulate matter in the outdoor environment, number concentrations of particles from vehicle emissions were measured at increasing distances from a major road. Particles in the size range from 0.015 to 0.697 μm were measured with the scanning mobility particle sizer (SMPS) and in the size range from 0.5 to 20 μm, with the aerodynamic particle sizer (APS). In addition to number concentration measurements, an approximation of PM2.5 fraction was obtained using a DustTrak (simple photometer). The measurements conducted at distances from the road ranging from 15 to 375 m showed, that for conditions where the wind is blowing directly from the road, the concentration of fine and ultrafine particles decays to around half of the maximum (measured at the closest point to the road) at a distance of approximately 100–150 m from the road. For the wind blowing parallel to the road, the reduction to half of the concentration occurs at 50–100 m. There is no effect on total particle number concentration at a distance greater than 15 m from the road when the wind is blowing towards the road and away from the sampling points. Total number concentrations of larger particles measured were not significantly higher than the average values for the urban environment, and decrease with distance from the road, reaching about 60% at 150 m from the road for wind from the road. PM2.5 levels also decrease with distance to around 75% for wind from the road and to 65% for wind parallel to the road, at a distance of 375 m.
Exposure to traffic-related air pollution (TRAP) contributes to increased cardiovascular risk. Land-use regression models can improve exposure assessment for TRAP.
We examined the association between medium-term concentrations of black carbon (BC) estimated by land-use regression and levels of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1), both markers of inflammatory and endothelial response.
We studied 642 elderly men participating in the Veterans Administration (VA) Normative Aging Study with repeated measurements of sICAM-1 and sVCAM-1 during 1999-2008. Daily estimates of BC exposure at each geocoded participant address were derived using a validated spatiotemporal model and averaged to form 4-, 8-, and 12-week exposures. We used linear mixed models to estimate associations, controlling for confounders. We examined effect modification by statin use, obesity, and diabetes.
We found statistically significant positive associations between BC and sICAM-1 for averages of 4, 8, and 12 weeks. An interquartile-range increase in 8-week BC exposure (0.30 μg/m3) was associated with a 1.58% increase in sICAM-1 (95% confidence interval, 0.18-3.00%). Overall associations between sVCAM-1 and BC exposures were suggestive but not statistically significant. We found a significant interaction with diabetes-where diabetics were more susceptible to the effect of BC-for both sICAM-1 and sVCAM-1. We also observed an interaction with statin use, which was statistically significant for sVCAM-1 and suggestive for sICAM-1. We found no evidence of an interaction with obesity.
Our results suggest that medium-term exposure to TRAP may induce an increased inflammatory/endothelial response, especially among diabetics and those not using statins.
Long- and short-term exposures to air pollution, especially fine particulate matter (PM(2.5)), have been linked to cardiovascular morbidity and mortality. One hypothesized mechanism for these associations involves microvascular effects. Retinal photography provides a novel, in vivo approach to examine the association of air pollution with changes in the human microvasculature.
Chronic and acute associations between residential air pollution concentrations and retinal vessel diameters, expressed as central retinal arteriolar equivalents (CRAE) and central retinal venular equivalents (CRVE), were examined using digital retinal images taken in Multi-Ethnic Study of Atherosclerosis (MESA) participants between 2002 and 2003. Study participants (46 to 87 years of age) were without clinical cardiovascular disease at the baseline examination (2000-2002). Long-term outdoor concentrations of PM(2.5) were estimated at each participant's home for the 2 years preceding the clinical exam using a spatio-temporal model. Short-term concentrations were assigned using outdoor measurements on the day preceding the clinical exam. Residential proximity to roadways was also used as an indicator of long-term traffic exposures. All associations were examined using linear regression models adjusted for subject-specific age, sex, race/ethnicity, education, income, smoking status, alcohol use, physical activity, body mass index, family history of cardiovascular disease, diabetes status, serum cholesterol, glucose, blood pressure, emphysema, C-reactive protein, medication use, and fellow vessel diameter. Short-term associations were further controlled for weather and seasonality. Among the 4,607 participants with complete data, CRAE were found to be narrower among persons residing in regions with increased long- and short-term levels of PM(2.5). These relationships were observed in a joint exposure model with -0.8 µm (95% confidence interval [CI] -1.1 to -0.5) and -0.4 µm (95% CI -0.8 to 0.1) decreases in CRAE per interquartile increases in long- (3 µg/m(3)) and short-term (9 µg/m(3)) PM(2.5) levels, respectively. These reductions in CRAE are equivalent to 7- and 3-year increases in age in the same cohort. Similarly, living near a major road was also associated with a -0.7 µm decrease (95% CI -1.4 to 0.1) in CRAE. Although the chronic association with CRAE was largely influenced by differences in exposure between cities, this relationship was generally robust to control for city-level covariates and no significant differences were observed between cities. Wider CRVE were associated with living in areas of higher PM(2.5) concentrations, but these findings were less robust and not supported by the presence of consistent acute associations with PM(2.5).
Residing in regions with higher air pollution concentrations and experiencing daily increases in air pollution were each associated with narrower retinal arteriolar diameters in older individuals. These findings support the hypothesis that important vascular phenomena are associated with small increases in short-term or long-term air pollution exposures, even at current exposure levels, and further corroborate reported associations between air pollution and the development and exacerbation of clinical cardiovascular disease. Please see later in the article for the Editors' Summary.
Cross-sectional studies suggest an association between exposure to ambient air pollution and atherosclerosis. We investigated the association between outdoor air quality and progression of subclinical atherosclerosis (common carotid artery intima-media thickness, CIMT).
We examined data from five double-blind randomized trials that assessed effects of various treatments on the change in CIMT. The trials were conducted in the Los Angeles area. Spatial models and land-use data were used to estimate the home outdoor mean concentration of particulate matter up to 2.5 micrometer in diameter (PM2.5), and to classify residence by proximity to traffic-related pollution (within 100 m of highways). PM2.5 and traffic proximity were positively associated with CIMT progression. Adjusted coefficients were larger than crude associations, not sensitive to modelling specifications, and statistically significant for highway proximity while of borderline significance for PM2.5 (P = 0.08). Annual CIMT progression among those living within 100 m of a highway was accelerated (5.5 micrometers/yr [95%CI: 0.13-10.79; p = 0.04]) or more than twice the population mean progression. For PM2.5, coefficients were positive as well, reaching statistical significance in the socially disadvantaged; in subjects reporting lipid lowering treatment at baseline; among participants receiving on-trial treatments; and among the pool of four out of the five trials.
Consistent with cross-sectional findings and animal studies, this is the first study to report an association between exposure to air pollution and the progression of atherosclerosis--indicated with CIMT change--in humans. Ostensibly, our results suggest that air pollution may contribute to the acceleration of cardiovascular disease development--the main causes of morbidity and mortality in many countries. However, the heterogeneity of the volunteering populations across the five trials, the limited sample size within trials and other relevant subgroups, and the fact that some key findings reached statistical significance in subgroups rather than the sample precludes generalizations to the general population.
Among patients with acute ischemic stroke, impaired kidney function has been shown to increase the mortality risk, but the shape of this relationship has not been evaluated in detail.
We estimated the glomerular filtration rate (eGFR) at the time of hospitalization in 1,175 consecutive patients hospitalized with acute ischemic stroke at the Beth Israel Deaconess Medical Center and examined the shape of the association between eGFR and all-cause mortality.
There were 508 deaths during a median follow-up of 40.3 months, resulting in a 'U'-shaped relationship between eGFR and all-cause mortality. The curve was relatively flat between 75 and 110 ml/min/1.73 m(2) but increased sharply at lower and higher levels of eGFR (test for nonlinearity: p < 0.0001).
Among patients with acute ischemic stroke, a reduced or highly elevated eGFR at hospital admission is associated with a higher mortality rate compared to patients with moderate levels of eGFR.
A cross the nation, government agencies, industries, and academic institutions are building high-containment biological laboratories to research hazardous pathogens that might accidentally or intentionally be introduced to the United States. Experts agree that the knowledge gained from such labs is a boon to public health—these are the places where the diagnostic test for Ebola virus, antitoxins for botulism, and therapies for multidrug-resistant tuberculosis were developed. But many of these same experts also point to the need for strict oversight of high-containment labs, and some worry that unchecked proliferation of such facilities increases the odds that study pathogens will make their way into the environment. The challenge for governing agencies is to provide researchers the flexibility to do their work while ensuring public safety.
In 2003, the Senate Committee on Governmental Affairs convened a hearing on the potential vulnerabilities of the U.S. food supply and agricultural sector to deliberate contamination. Two years earlier, the United Kingdom had experienced an epidemic of foot-and-mouth disease (FMD) that devastated the British livestock industry. The disease was not introduced intentionally, but many found the timing disquieting, given the subsequent events of 9/11 and deaths later that fall from anthrax sent through the mail. The U.S. agricultural sector accounts for 13% of the gross domestic product and is vulnerable to both intentional and accidental introduction of infectious disease, according to Lawrence Dyckman, director of natural resources and environment for the U.S. Government Accountability Office (GAO). In testimony at the 2003 hearing, Dyckman identified more than 40 contagious foreign animal diseases as threats to the U.S. agricultural economy.
This vulnerability prompted President George W. Bush to issue Homeland Security Presidential Directive 9 in 2004. Among other provisions, the directive called for the secretaries of the U.S. Department of Agriculture (USDA) and Department of Homeland Security (DHS) to develop secure, state-of-the-art biocontainment laboratories to research and develop diagnostic capabilities for exotic animal diseases, including “zoonotic” diseases that can be transmitted to humans.
Three years later, the House Energy and Commerce Subcommittee on Oversight and Investigations held a hearing on the proliferation and oversight of high-containment labs. In testimony before the subcommittee, Gigi Kwik Gronvall, a senior associate with the Center for Biosecurity of the University of Pittsburgh Medical Center, said, “Protecting the nation against destabilizing large-scale epidemics, whether natural or man-made, is an urgent priority. . . . [N]ew high-containment laboratories are necessary if we are to produce the scientific advances needed to develop medical countermeasures against bioweapons and emerging diseases.” At the same time, said Gronvall and other witnesses, the need for rigorous oversight and training of personnel is paramount.
Associations between cardiovascular mortality and air pollution and noise together were investigated.
Data from the ongoing Netherlands Cohort Study on Diet and Cancer (120,852 subjects; follow-up 1987-1996) were used. Cox proportional hazard analyses were conducted for the association between cardiovascular mortality and exposure to black smoke, traffic intensity on the nearest road and road traffic noise at the home address.
The correlations between traffic noise and background black smoke, and traffic intensity on the nearest road were moderate at 0.24 and 0.30, respectively. Traffic intensity was associated with cardiovascular mortality, with highest relative risk (95% confidence interval) for ischaemic heart disease (IHD) mortality being 1.11 (1.03 to 1.20) (increment 10,000 motor vehicles/24 h). Relative risks for black smoke concentrations were elevated for cerebrovascular (1.39 (0.99 to 1.94)) and heart failure mortality (1.75 (1.00 to 3.05)) (increment 10 microg/m(3)). These associations were insensitive to adjustment for traffic noise. There was an excess of cardiovascular mortality in the highest noise category (>65 dB(A)), with elevated risks for IHD (1.15 (0.86 to 1.53)) and heart failure mortality (1.99 (1.05 to 3.79)). After adjustment for black smoke and traffic intensity, noise risk reduced to unity for IHD mortality and was slightly reduced for heart failure mortality.
Associations between black smoke concentrations and traffic intensity on the nearest road with specific cardiovascular causes of death were not explained by traffic noise in this study.
Because human activities impact the timing, location, and degree of pollutant exposure, they play a key role in explaining exposure variation. This fact has motivated the collection of activity pattern data for their specific use in exposure assessments. The largest of these recent efforts is the National Human Activity Pattern Survey (NHAPS), a 2-year probability-based telephone survey (
n=9386) of exposure-related human activities in the United States (U.S.) sponsored by the U.S. Environmental Protection Agency (EPA). The primary purpose of NHAPS was to provide comprehensive and current exposure information over broad geographical and temporal scales, particularly for use in probabilistic population exposure models. NHAPS was conducted on a virtually daily basis from late September 1992 through September 1994 by the University of Maryland's Survey Research Center using a computer-assisted telephone interview instrument (CATI) to collect 24-h retrospective diaries and answers to a number of personal and exposure-related questions from each respondent. The resulting diary records contain beginning and ending times for each distinct combination of location and activity occurring on the diary day (i.e., each microenvironment). Between 340 and 1713 respondents of all ages were interviewed in each of the 10 EPA regions across the 48 contiguous states. Interviews were completed in 63% of the households contacted. NHAPS respondents reported spending an average of 87% of their time in enclosed buildings and about 6% of their time in enclosed vehicles. These proportions are fairly constant across the various regions of the U.S. and Canada and for the California population between the late 1980s, when the California Air Resources Board (CARB) sponsored a state-wide activity pattern study, and the mid-1990s, when NHAPS was conducted. However, the number of people exposed to environmental tobacco smoke (ETS) in California seems to have decreased over the same time period, where exposure is determined by the reported time spent with a smoker. In both California and the entire nation, the most time spent exposed to ETS was reported to take place in residential locations.
The objective of this study was to determine if there is an exposure gradient in particulate matter concentrations for people living near interstate highways, and to determine how far from the highway the gradient extends. Air samples were collected in a residential area of Greater Cincinnati in the vicinity of two major highways. The measurements were conducted at different distances from the highways by using ultrafine particle counters (measurement range: 0.02-1 microm), optical particle counters (0.3-20 microm), and PM2.5 Harvard Impactors (0.02-2.5 microm). The collected PM2.5 samples were analyzed for mass concentration, for elemental and organic carbon, and for elemental concentrations. The results show that the aerosol concentration gradient was most clearly seen in the particle number concentration measured by the ultrafine particle counters. The concentration of ultrafine particles decreased to half between the sampling points located at 50 m and 150 m downwind from the highway. Additionally, elemental analysis revealed a gradient in sulfur concentrations up to 400 m from the highway in a residential area that does not have major nearby industrial sources. This gradient was qualitatively attributed to the sulfate particle emissions from diesel engine exhausts, and was supported by the concentration data on several key elements indicative of traffic sources (road dust and diesel exhaust). As different particulate components gave different profiles of the diesel exposure gradient, these results indicate that no single element or component of diesel exhaust can be used as a surrogate for diesel exposure, but more comprehensive signature analysis is needed. This characterization is crucial especially when the exposure data are to be used in epidemiological studies.
Associations have been found between long-term exposure to ambient air pollution and cardiovascular morbidity and mortality. The contribution of air pollution to atherosclerosis that underlies many cardiovascular diseases has not been investigated. Animal data suggest that ambient particulate matter (PM) may contribute to atherogenesis. We used data on 798 participants from two clinical trials to investigate the association between atherosclerosis and long-term exposure to ambient PM up to 2.5 microm in aerodynamic diameter (PM2.5). Baseline data included assessment of the carotid intima-media thickness (CIMT), a measure of subclinical atherosclerosis. We geocoded subjects' residential areas to assign annual mean concentrations of ambient PM2.5. Exposure values were assigned from a PM2.5 surface derived from a geostatistical model. Individually assigned annual mean PM2.5 concentrations ranged from 5.2 to 26.9 microg/m3 (mean, 20.3). For a cross-sectional exposure contrast of 10 microg/m3 PM2.5, CIMT increased by 5.9% (95% confidence interval, 1-11%). Adjustment for age reduced the coefficients, but further adjustment for covariates indicated robust estimates in the range of 3.9-4.3% (p-values, 0.05-0.1). Among older subjects (greater than or equal to 60 years of age), women, never smokers, and those reporting lipid-lowering treatment at baseline, the associations of PM2.5 and CIMT were larger with the strongest associations in women 60 years of age (15.7%, 5.7-26.6%). These results represent the first epidemiologic evidence of an association between atherosclerosis and ambient air pollution. Given the leading role of cardiovascular disease as a cause of death and the large populations exposed to ambient PM2.5, these findings may be important and need further confirmation.
Recent studies have suggested a link between inhaled particulate matter exposure in urban areas and susceptibility to cardiovascular events; however, the precise mechanisms remain to be determined.
To test the hypothesis that subchronic exposure to environmentally relevant particulate matter, even at low concentrations, potentiates atherosclerosis and alters vasomotor tone in a susceptible disease model.
Between July 21, 2004, and January 12, 2005, 28 apolipoprotein E-/- (apoE-/-) mice were, based on randomized assignments, fed with normal chow or high-fat chow and exposed to concentrated ambient particles of less than 2.5 microm (PM2.5) or filtered air (FA) in Tuxedo, NY, for 6 hours per day, 5 days per week for a total of 6 months.
Composite atherosclerotic plaque in the thoracic and abdominal aorta and vasomotor tone changes.
In the high-fat chow group, the mean (SD) composite plaque area of PM2.5 vs FA was 41.5% (9.8%) vs 26.2% (8.6%), respectively (P<.001); and in the normal chow group, the composite plaque area was 19.2% (13.1%) vs 13.2% (8.1%), respectively (P = .15). Lipid content in the aortic arch measured by oil red-O staining revealed a 1.5-fold increase in mice fed the high-fat chow and exposed to PM2.5 vs FA (30.0 [8.2] vs 20.0 [7.0]; 95% confidence interval [CI], 1.21-1.83; P = .02). Vasoconstrictor responses to phenylephrine and serotonin challenge in the thoracic aorta of mice fed high-fat chow and exposed to PM2.5 were exaggerated compared with exposure to FA (mean [SE], 134.2% [5.2%] vs 100.9% [2.9%], for phenylephrine, and 156.0% [5.6%] vs 125.1% [7.5%], for serotonin; both P = .03); relaxation to the endothelium-dependent agonist acetylcholine was attenuated (mean [SE] of half-maximal dose for dilation, 8.9 [0.2] x 10(-8) vs 4.3 [0.1] x 10(-8), respectively; P = .04). Mice fed high-fat chow and exposed to PM2.5 demonstrated marked increases in macrophage infiltration, expression of the inducible isoform of nitric oxide synthase, increased generation of reactive oxygen species, and greater immunostaining for the protein nitration product 3-nitrotyrosine (all P<.001).
In an apoE-/- mouse model, long-term exposure to low concentration of PM2.5 altered vasomotor tone, induced vascular inflammation, and potentiated atherosclerosis.
Long-term exposure to particulate air pollution has been associated with an increased risk of dying from cardiopulmonary and ischemic heart disease, yet few studies have evaluated cardiovascular end points other than mortality. We investigated the relationship between long-term exposure to traffic and occurrence of acute myocardial infarction (AMI) in a case-control study.
A total of 5,049 confirmed cases of AMI were identified between 1995 and 2003 as part of the Worcester Heart Attack Study, a community-wide study examining changes over time in the incidence of AMI among greater Worcester, Massachusetts, residents. Population controls were selected from Massachusetts resident lists. We used cumulative traffic within 100 m of subjects' residence and distance from major roadway as proxies for exposure to traffic-related air pollution. We estimated the relationship between exposure to traffic and occurrence of AMI using logistic regression, and we adjusted for the following potential confounders: age, sex, section of the study area, point sources emissions of particulate matter with aerodynamic diameter < 2.5 microm, area socioeconomic characteristics, and percentage of open space.
An increase in cumulative traffic near the home was associated with a 4% increase in the odds of AMI per interquartile range [95% confidence interval (CI), 2-7%], whereas living near a major roadway was associated with a 5% increase in the odds of AMI per kilometer (95% CI, 3-6%).
These results provide support for an association between long-term exposure to traffic and the risk of AMI.
Understanding mechanistic pathways linking airborne particle exposure to cardiovascular health is important for causal inference and setting environmental standards. We evaluated whether urinary albumin excretion, a subclinical marker of microvascular function which predicts cardiovascular events, was associated with ambient particle exposure.
Urinary albumin and creatinine were measured among members of the Multi-Ethnic Study of Atherosclerosis at three visits during 2000-2004. Exposure to PM(2.5) and PM(10) (microg/m(3)) was estimated from ambient monitors for 1 month, 2 months and two decades before visit one. We regressed recent and chronic (20 year) particulate matter (PM) exposure on urinary albumin/creatinine ratio (UACR, mg/g) and microalbuminuria at first examination, controlling for age, race/ethnicity, sex, smoking, second-hand smoke exposure, body mass index and dietary protein (n = 3901). We also evaluated UACR changes and development of microalbuminuria between the first, and second and third visits which took place at 1.5- to 2-year intervals in relation to chronic PM exposure prior to baseline using mixed models.
Chronic and recent particle exposures were not associated with current UACR or microalbuminuria (per 10 microg/m(3) increment of chronic PM(10) exposure, mean difference in log UACR = -0.02 (95% CI -0.07 to 0.03) and relative probability of having microalbuminuria = 0.92 (95% CI 0.77 to 1.08)) We found only weak evidence that albuminuria was accelerated among those chronically exposed to particles: each 10 microg/m(3) increment in chronic PM(10) exposure was associated with a 1.14 relative probability of developing microalbuminuria over 3-4 years, although 95% confidence intervals included the null (95% CI 0.96 to 1.36).
UACR is not a strong mechanistic marker for the possible influence of air pollution on cardiovascular health in this sample.
Exposure to airborne particulate matter has been linked to cardiovascular events. Whether this finding reflects an effect of particulate matter exposure on the triggering of events or development of atherosclerosis remains unknown. Using data from the Multi-Ethnic Study of Atherosclerosis collected at baseline (2000-2002), the authors investigated associations of 20-year exposures to particulate matter with measures of subclinical disease (coronary calcium, common carotid intimal-medial thickness, and ankle-brachial index) in 5,172 US adults without clinical cardiovascular disease. Particulate matter exposures for the 20 years prior to assessment of subclinical disease were obtained from a space-time model of Environmental Protection Agency monitor data linked to residential history data for each participant. Intimal-medial thickness was weakly, positively associated with exposures to particulate matter <10 microm in aerodynamic diameter and <2.5 microm in aerodynamic diameter after controlling for age, sex, race/ethnicity, socioeconomic factors, diet, smoking, physical activity, blood lipids, diabetes, hypertension, and body mass index (1-4% increase per 21-microg/m(3) increase in particulate matter <10 microm in aerodynamic diameter or a 12.5-microg/m(3) increase in particulate matter <2.5 microm in aerodynamic diameter). No consistent associations with other measures of atherosclerosis were observed. There was no evidence of effect modification by sociodemographic factors, lipid status, smoking, diabetes, body mass index, or site. Results are compatible with some effect of particulate matter exposures on development of carotid atherosclerosis.
Decreased glomerular filtration rate (GFR) and albuminuria are used in combination to define chronic kidney disease, but their separate and combined effects on cardiovascular and all-cause mortality have not been studied in the general population. The linked mortality file of the Third National Health and Nutrition Examination Survey includes data from 13 years of follow-up (1988-2000) for 14,586 US adults. The authors estimated GFR from standardized serum creatinine levels. Albuminuria was defined by the urinary albumin:creatinine ratio. Incidence rate ratios (IRRs) were adjusted for major cardiovascular disease risk factors and C-reactive protein. Lower estimated GFR was associated with higher risks of cardiovascular and all-cause mortality overall and within every albuminuria category. Likewise, increasing albuminuria was associated with higher risk of estimated GFR overall and within every category. When estimated GFR and albuminuria were examined simultaneously, a 10-ml/minute/1.73 m(2) lower estimated GFR (among persons with estimated GFR <60 ml/minute/1.73 m(2)) was associated with an IRR of 1.29 (95% confidence interval: 1.06, 1.55) for cardiovascular mortality and a doubling of albuminuria was associated with an IRR of 1.06 (95% confidence interval: 1.04, 1.08) for cardiovascular mortality. The authors conclude that moderately decreased estimated GFR and albuminuria independently predict cardiovascular and all-cause mortality in the general population. These data support recent recommendations defining chronic kidney disease and stratifying subsequent risks based on both decreased GFR and albuminuria.
Blood pressure (BP) may be implicated in associations observed between ambient particulate matter and cardiovascular morbidity and mortality. This study examined cross-sectional associations between short-term ambient fine particles (particulate matter <or= 2.5 microm in aerodynamic diameter; PM(2.5)) and BP: systolic (SBP), diastolic (DBP), mean arterial (MAP), and pulse pressure (PP).
The study sample included 5,112 persons 45-84 years of age, free of cardiovascular disease at the Multi-Ethnic Study of Atherosclerosis baseline examination (2000-2002). Data from U.S. Environmental Protection Agency monitors were used to estimate ambient PM(2.5) exposures for the preceding 1, 2, 7, 30, and 60 days. Roadway data were used to estimate local exposures to traffic-related particles.
Results from linear regression found PP and SBP positively associated with PM(2.5). For example, a 10-microg/m(3) increase in PM(2.5) 30-day mean was associated with 1.12 mmHg higher pulse pressure [95% confidence interval (CI), 0.28-1.97] and 0.99 mmHg higher systolic BP (95% CI, -0.15 to 2.13), adjusted for age, sex, race/ethnicity, income, education, body mass index, diabetes, cigarette smoking and environmental tobacco smoke, alcohol use, physical activity, medications, atmospheric pressure, and temperature. Results were much weaker and not statistically significant for MAP and DBP. Although traffic-related variables were not themselves associated with BP, the association between PM(2.5) and BP was stronger in the presence of higher traffic exposure.
Higher SBP and PP were associated with ambient levels of PM(2.5) and the association was stronger in the presence of roadway traffic, suggesting that impairment of blood pressure regulation may play a role in response to air pollution.
Although patients with heart failure (HF) have been identified as particularly susceptible to the acute effects of air pollution, the effects of long-term exposure to air pollution on patients with this increasingly prevalent disease are largely unknown.
This study was designed to examine the mortality risk associated with residential exposure to traffic-related air pollution among HF patients.
A total of 1,389 patients hospitalized with acute HF in greater Worcester, Massachusetts, during 2000 were followed for survival through December 2005. We used daily traffic within 100 and 300 m of residence as well as the distance from residence to major roadways and to bus routes as proxies for residential exposure to traffic-related air pollution. We assessed mortality risks for each exposure variable using Cox proportional hazards models adjusted for prognostic factors.
After the 5-year follow-up, only 334 (24%) subjects were still alive. An interquartile range increase in daily traffic within 100 m of home was associated with a mortality hazard ratio (HR) of 1.15 [95% confidence interval (CI), 1.05-1.25], whereas for traffic within 300 m this association was 1.09 (95% CI, 1.01-1.19). The mortality risk decreased with increasing distance to bus routes (HR = 0.88; 95% CI, 0.81-0.96) and was larger for those living within 100 m of a major roadway or 50 m of a bus route (HR = 1.30; 95% CI, 1.13-1.49). Adjustment for area-based income and educational level slightly attenuated these associations.
Residential exposure to traffic-related air pollution increases the mortality risk after hospitalization with acute HF. Reducing exposure to traffic-related emissions may improve the long-term prognosis of HF patients.
Chronic kidney disease1 (CKD) is a worldwide public health problem. In the United States, there is a rising incidence and prevalence of kidney failure, with poor outcomes and high cost. The number of individuals with kidney failure treated by dialysis and transplantation exceeded 320 000 in 1998 and is expected to surpass 650 000 by 2010.1,2 There is an even higher prevalence of earlier stages of CKD (Table 1).1,3 Kidney failure requiring treatment with dialysis or transplantation is the most visible outcome of CKD. However, cardiovascular disease (CVD) is also frequently associated with CKD, which is important because individuals with CKD are more likely to die of CVD than to develop kidney failure,4 CVD in CKD is treatable and potentially preventable, and CKD appears to be a risk factor for CVD. In 1998, the National Kidney Foundation (NKF) Task Force on Cardiovascular Disease in Chronic Renal Disease issued a report emphasizing the high risk of CVD in CKD.5 This report showed that there was a high prevalence of CVD in CKD and that mortality due to CVD was 10 to 30 times higher in dialysis patients than in the general population (Figure 1 and Table 2).6–18 The task force recommended that patients with CKD be considered in the “highest risk group” for subsequent CVD events and that treatment recommendations based on CVD risk stratification should take into account the highest-risk status of patients with CKD.
View this table:
TABLE 1. Stages of CKD
Figure 1. Cardiovascular mortality defined by death due to arrhythmias, cardiomyopathy, cardiac arrest, myocardial infarction, atherosclerotic heart disease, and pulmonary edema in general population (GP; National Center for Health Statistics [NCHS] multiple cause of mortality data files International Classification of Diseases, 9th Revision [ICD 9] codes 402, 404, 410 to 414, and …
Background
Equations to estimate glomerular filtration rate (GFR) are routinely used to assess kidney function. Current equations have limited precision and systematically underestimate measured GFR at higher levels.
The relationship between residential proximity to roadway and long-term survival after acute myocardial infarction (AMI) is unknown. We investigated the association between distance from residence and major roadway and 10-year all-cause mortality after AMI in the Determinants of Myocardial Infarction Onset Study (Onset Study), hypothesizing that living closer to a major roadway at the time of AMI would be associated with increased risk of mortality.
The Onset Study enrolled 3886 individuals hospitalized for AMI in 64 centers across the United States from 1989 to 1996. Institutionalized patients, those providing only post office boxes, and those whose addresses could not be geocoded were excluded, leaving 3547 patients eligible for analysis. Addresses were geocoded, and distance to the nearest major roadway was assigned. Cox regression was used to calculate hazard ratios, with adjustment for personal characteristics (age, sex, race, education, marital status, distance to nearest acute care hospital), clinical characteristics (smoking, body mass index, comorbidities, medications), and neighborhood-level characteristics derived from US Census block group data (household income, education, urbanicity). There were 1071 deaths after 10 years of follow-up. In the fully adjusted model, compared with living >1000 m, hazard ratios (95% confidence interval) for living ≤100 m were 1.27 (1.01-1.60), for 100 to ≤200 m were 1.19 (0.93-1.60), and for 200 to ≤1000 m were 1.13 (0.99-1.30) (P(trend)=0.016).
In this multicenter study, living close to a major roadway at the time of AMI was associated with increased risk of all-cause 10-year mortality; this relationship persisted after adjustment for individual and neighborhood-level covariates.
A method is described of calculating the sound pressure level received from single, representative light and heavy vehicles after propagation over terrain composed of various combinations of hard ground and grass-land. These results are then used to derive correction contours for the attenuation with distance of the Leq level received from streams of each class of vehicle. The results apply to conditions where the boundary between the soft and hard areas is parallel to the traffic stream and the soft ground is on the receiver side. Various positions of the boundary are considered. A simple prediction method for Leq is developed, incorporating the distance corrections. Similar calculations are carried out for the attenuation with distance of the L10 noise index for a representative stream of vehicles. Based on these results simple prediction equations for the excess attenuation are proposed in terms of the receiver position and the proportion of soft ground below the propagation path.
Road traffic noise is an important source of noise annoyance in the community. We performed a meta-analysis to assess whether there is an association between noise annoyance from road traffic noise and cardiovascular diseases (arterial hypertension and ischemic heart disease) in adult population. The meta-analysis included studies that: a. had noise annoyance as exposure, quantified either as "annoyed versus non-annoyed" or with various scales collected by standardized questionnaires; b. arterial hypertension or ischemic heart disease as outcome; c. had included only adult population (age >18 years); d. the studies had to have as effect size odds ratios or relative risk. From the individual studies those odds ratios were selected for meta-analysis which compared most distant categories. Eight studies that fulfilled criteria published between 1992 and 2006 were included in the meta-analysis: 6 studies had a cross-sectional design, 1 study had a case-control-design and 1 study had a cohort design. Increased annoyance was significantly associated with arterial hypertension (pooled risk estimate = 1.16, 95% confidence interval 1.02-1.29) while the association with ischemic heart disease did not reach statistical significance (pooled risk estimate = 1.07, 95% confidence interval 0.99-1.14). No publication bias was evidenced. The results of this meta-analysis demonstrated the existence of a positive and significant association between noise annoyance from road traffic and the risk of arterial hypertension and a positive yet insignificant association between noise annoyance and the risk of ischemic heart disease.
Epidemiological studies suggest that long-term exposure to road traffic noise increases the risk of cardiovascular disorders. The aim of this study was to investigate the relation between exposure to road traffic noise and risk for stroke, which has not been studied before.
In a population-based cohort of 57,053 people, we identified 1881 cases of first-ever stroke in a national hospital register between 1993-1997 and 2006. Exposure to road traffic noise and air pollution during the same period was estimated for all cohort members from residential address history. Associations between exposure to road traffic noise and stroke incidence were analysed in a Cox regression model with stratification for gender and calendar-year and adjustment for air pollution and other potential confounders. We found an incidence rate ratio (IRR) of 1.14 for stroke [95% confidence interval (CI): 1.03-1.25] per 10 dB higher level of road traffic noise (L(den)). There was a statistically significant interaction with age (P < 0.001), with a strong association between road traffic noise and stroke among cases over 64.5 years (IRR: 1.27; 95% CI: 1.13-1.43) and no association for those under 64.5 years (IRR: 1.02; 95% CI: 0.91-1.14).
Exposure to residential road traffic noise was associated with a higher risk for stroke among people older than 64.5 years of age.
The aim of this study was to investigate the association of long-term residential exposure to fine particles with carotid intima-media thickness (CIMT).
Experimental and epidemiological evidence suggest that long-term exposure to air pollution might have a causal role in atherogenesis, but epidemiological findings are still inconsistent. We investigate whether urban particulate matter (PM) air pollution is associated with CIMT, a marker of subclinical atherosclerosis.
We used baseline data (2000 to 2003) from the HNR (Heinz Nixdorf Recall) study, a population-based cohort of 4,814 participants, 45 to 75 years of age. We assessed residential long-term exposure to PM with a chemistry transport model and measured distance to high traffic. Multiple linear regression was used to estimate associations of air pollutants and traffic with CIMT, adjusting for each other, city of residence, age, sex, diabetes, and lifestyle variables.
Median CIMT of the 3,380 analyzed participants was 0.66 mm (interquartile range 0.16 mm). An interdecile range increase in PM(2.5) (4.2 μg/m(3)), PM(10) (6.7 μg/m(3)), and distance to high traffic (1,939 m) was associated with a 4.3% (95% confidence interval [CI]: 1.9% to 6.7%), 1.7% (95% CI: -0.7% to 4.1%), and 1.2% (95% CI: -0.2% to 2.6%) increase in CIMT, respectively.
Our study shows a clear association of long-term exposure to PM(2.5) with atherosclerosis. This finding strengthens the hypothesized role of PM(2.5) as a risk factor for atherogenesis.
In 2004, the first American Heart Association scientific statement on "Air Pollution and Cardiovascular Disease" concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM <2.5 microm in diameter (PM(2.5)) over a few hours to weeks can trigger cardiovascular disease-related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM(2.5) exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM(2.5) exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality.
The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) recently published an equation for estimated glomerular filtration rate (eGFR) using the same variables (serum creatinine level, age, sex, and race) as the Modification of Diet in Renal Disease (MDRD) Study equation. Although the CKD-EPI equation estimates GFR more precisely compared with the MDRD Study equation, whether this equation improves risk prediction is unknown.
Prospective cohort study, the Atherosclerosis Risk in Communities (ARIC) Study.
13,905 middle-aged participants without a history of cardiovascular disease with median follow-up of 16.9 years.
eGFR.
We compared the association of eGFR in categories (>or=120, 90-119, 60-89, 30-59, and <30 mL/min/1.73 m(2)) using the CKD-EPI and MDRD Study equations with risk of incident end-stage renal disease, all-cause mortality, coronary heart disease, and stroke.
The median value for eGFR(CKD-EPI) was higher than that for eGFR(MDRD) (97.6 vs 88.8 mL/min/1.73 m(2); P < 0.001). The CKD-EPI equation reclassified 44.9% (n = 3,079) and 43.5% (n = 151) of participants with eGFR(MDRD) of 60-89 and 30-59 mL/min/1.73 m(2), respectively, upward to a higher eGFR category, but reclassified no one with eGFR(MDRD) of 90-119 or <30 mL/min/1.73 m(2), decreasing the prevalence of CKD stages 3-5 from 2.7% to 1.6%. Participants with eGFR(MDRD) of 30-59 mL/min/1.73 m(2) who were reclassified upward had lower risk compared with those who were not reclassified (end-stage renal disease incidence rate ratio, 0.10 [95% CI, 0.03-0.33]; all-cause mortality, 0.30 [95% CI, 0.19-0.48]; coronary heart disease, 0.36 [95% CI, 0.21-0.61]; and stroke, 0.50 [95% CI, 0.24-1.02]). Similar results were observed for participants with eGFR(MDRD) of 60-89 mL/min/1.73 m(2). More frequent reclassification of younger, female, and white participants explained some of these trends. Net reclassification improvement in participants with eGFR < 120 mL/min/1.73 m(2) was positive for all outcomes (P < 0.001).
Limited number of cases with eGFR < 60 mL/min/1.73 m(2) and no measurement of albuminuria.
The CKD-EPI equation more appropriately categorized individuals with respect to long-term clinical risk compared with the MDRD Study equation, suggesting improved clinical usefulness in this middle-aged population.
Particulate air pollution has been consistently linked to increased risk of arterial cardiovascular disease. Few data on air pollution exposure and risk of venous thrombosis are available. We investigated whether living near major traffic roads increases the risk of deep vein thrombosis (DVT), using distance from roads as a proxy for traffic exposure.
From 1995 through 2005, we examined 663 patients with DVT of the lower limbs and 859 age-matched controls from cities with population >15 000 inhabitants in Lombardia Region, Italy. We assessed distance from residential addresses to the nearest major traffic road using geographic information system methodology. The risk of DVT was estimated from logistic regression models adjusting for multiple clinical and environmental covariates. The risk of DVT was increased (odds ratio=1.33; 95% confidence interval, 1.03 to 1.71; P=0.03 in age-adjusted models; odds ratio=1.47; 95% confidence interval, 1.10 to 1.96; P=0.008 in models adjusted for multiple covariates) for subjects living near a major traffic road (index distance of 3 meters, 10th centile of the distance distribution) compared with those living farther away (reference distance of 245 meters, 90th centile). The increase in DVT risk was approximately linear over the observed distance range (from 718 to 0 meters) and was not modified after adjusting for
=0.008 for 10th versus 90th distance centile in models adjusting for area levels of particulate matter <10 mum in aerodynamic diameter in the year before diagnosis).
Living near major traffic roads is associated with increased risk of DVT.
Equations to estimate glomerular filtration rate (GFR) are routinely used to assess kidney function. Current equations have limited precision and systematically underestimate measured GFR at higher values.
To develop a new estimating equation for GFR: the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation.
Cross-sectional analysis with separate pooled data sets for equation development and validation and a representative sample of the U.S. population for prevalence estimates.
Research studies and clinical populations ("studies") with measured GFR and NHANES (National Health and Nutrition Examination Survey), 1999 to 2006.
8254 participants in 10 studies (equation development data set) and 3896 participants in 16 studies (validation data set). Prevalence estimates were based on 16,032 participants in NHANES.
GFR, measured as the clearance of exogenous filtration markers (iothalamate in the development data set; iothalamate and other markers in the validation data set), and linear regression to estimate the logarithm of measured GFR from standardized creatinine levels, sex, race, and age.
In the validation data set, the CKD-EPI equation performed better than the Modification of Diet in Renal Disease Study equation, especially at higher GFR (P < 0.001 for all subsequent comparisons), with less bias (median difference between measured and estimated GFR, 2.5 vs. 5.5 mL/min per 1.73 m(2)), improved precision (interquartile range [IQR] of the differences, 16.6 vs. 18.3 mL/min per 1.73 m(2)), and greater accuracy (percentage of estimated GFR within 30% of measured GFR, 84.1% vs. 80.6%). In NHANES, the median estimated GFR was 94.5 mL/min per 1.73 m(2) (IQR, 79.7 to 108.1) vs. 85.0 (IQR, 72.9 to 98.5) mL/min per 1.73 m(2), and the prevalence of chronic kidney disease was 11.5% (95% CI, 10.6% to 12.4%) versus 13.1% (CI, 12.1% to 14.0%).
The sample contained a limited number of elderly people and racial and ethnic minorities with measured GFR.
The CKD-EPI creatinine equation is more accurate than the Modification of Diet in Renal Disease Study equation and could replace it for routine clinical use.
National Institute of Diabetes and Digestive and Kidney Diseases.
Long-term exposure to particulate air pollution has been associated with increased cardiovascular disease. Biologic pathways for this association are not fully understood.
We examined the association of urban air pollution with atherosclerosis of the peripheral vascular bed, using baseline data (2000-2003) from 4348 participants in a population-based cohort study in the German Ruhr Area. Levels of annual fine particulate matter (PM2.5) exposure, derived from a dispersion and chemistry transport model, were assigned to the participants' home addresses. Residential traffic exposure was assessed by the distance between residence and major roads (federal and state highways). Using multiple regression analyses and controlling for individual level risk factors, we examined the association of PM2.5 and traffic with the ankle-brachial index and prevalence of peripheral arterial disease, defined as an index of less than 0.9 or a history of treatment for peripheral artery disease.
Living within 101-200, 51-100, and 50 m of a major road was associated with an adjusted absolute decrease in ankle-brachial index of -0.015 (95% confidence interval [CI] = -0.030 to 0.0), -0.002 (-0.021 to 0.016) and -0.024 (-0.047 to -0.001), respectively. Stronger associations were seen in women, whereas no clear association was found in men. Individuals living within 50 m of a major road had an OR of 1.77 (1.01-2.1) for peripheral arterial disease compared with those living more than 200 m away. Associations with PM2.5 were inconsistent.
This study adds to the evidence that long-term residential exposure to traffic is associated with atherosclerosis.
Traffic noise is ubiquitous in many communities and is an important environmental concern, especially for persons located near major roadways. Several different methods are available to estimate noise levels resulting from roadway traffic. These include computational, graphical, and computer modeling techniques. The prediction methodology presented here is a simplified technique that can be used for estimating noise resulting from traffic and for screening traffic noise impacts. This Traffic Noise Screening (TNS) approach consists of a series of traffic noise level prediction graphs developed for different roadway configurations. The graphs are based on the results from using the Federal Highway Administration (FHWA) STAMINA2.0 computerized noise prediction model for various scenarios. Data inputs to the TNS approach include roadway genometries, traffic volumes, vehicle travel speed, and centerline distance to the receptors. The TNS graphs allow easy estimation of traffic noise levels for use in predicting traffic-related noise impacts. This TNS approach is not intended as a substitute for detailed modeling, such as with STAMINA2.0, but as a screening tool to aid in determining when detailed modeling may be necessary. If screening results indicate that noise estimates are significant, or if the scenario is rather complex, then additional, more detailed modeling can be performed.
We sought to determine the effect of exposure to air pollution particulate matter <10 microm (PM(10)) on the progression of atherosclerosis in rabbits.
Epidemiologic studies have associated exposure to ambient PM(10) with increased cardiovascular morbidity and mortality. We have previously shown that PM(10) exposure induces a systemic inflammatory response that includes marrow stimulation, and we hypothesized that this response accelerates atherosclerosis.
Watanabe heritable hyperlipidemic rabbits were exposed to PM(10) (n = 10) or vehicle (n = 6) for four weeks, and bone marrow stimulation was measured. Quantitative histologic methods were used to determine the morphologic features of the atherosclerotic lesions.
Exposure to PM(10) caused an increase in circulating polymorphonuclear leukocytes (PMN) band cell counts (day 15: 24.6 +/- 3.0 vs. 11.5 +/- 2.7 x 10(7)/l [PM(10) vs. vehicle], p < 0.01) and an increase in the size of the bone marrow mitotic pool of PMNs. Exposure to PM(10) also caused progression of atherosclerotic lesions toward a more advanced phenotype. The volume fraction (vol/vol) of the coronary atherosclerotic lesions was increased by PM(10) exposure (33.3 +/- 4.6% vs. 19.5 +/- 3.1% [PM(10) vs. vehicle], p < 0.05). The vol/vol of atherosclerotic lesions correlated with the number of alveolar macrophages that phagocytosed PM(10) (coronary arteries: r = 0.53, p < 0.05; aorta: r = 0.51, p < 0.05). Exposure to PM(10) also caused an increase in plaque cell turnover and extracellular lipid pools in coronary and aortic lesions, as well as in the total amount of lipids in aortic lesions.
Progression of atherosclerosis and increased vulnerability to plaque rupture may underlie the relationship between particulate air pollution and excess cardiovascular death.
Recently developed clinical practice guidelines and calibration of the Third National Health and Nutrition Examination Survey (NHANES III) serum creatinine assay provide a basis for estimating the prevalence and distribution of chronic kidney disease (CKD) in the United States using standardized criteria based on estimated glomerular filtration rate (GFR) and persistent albuminuria.
A nationally representative sample of 15,625 noninstitutionalized adults aged 20 years and older from the NHANES III was analyzed. Kidney function (GFR), kidney damage (albuminuria), and stages of CKD (GFR and albuminuria) were estimated from calibrated serum creatinine level, spot urine albumin level, age, sex, and race. GFR was estimated using the simplified Modification of Diet in Renal Disease Study equation and compared with the Cockcroft-Gault equation for creatinine clearance (CCr).
The prevalence of CKD in the US adult population was 11% (19.2 million). By stage, an estimated 5.9 million individuals (3.3%) had stage 1 (persistent albuminuria with a normal GFR), 5.3 million (3.0%) had stage 2 (persistent albuminuria with a GFR of 60 to 89 mL/min/1.73 m(2)), 7.6 million (4.3%) had stage 3 (GFR, 30 to 59 mL/min/1.73 m(2)), 400,000 individuals (0.2%) had stage 4 (GFR, 15 to 29 mL/min/1.73 m(2)), and 300,000 individuals (0.2%) had stage 5, or kidney failure. Aside from hypertension and diabetes, age is a key predictor of CKD, and 11% of individuals older than 65 years without hypertension or diabetes had stage 3 or worse CKD. Compared with GFR estimates, CCr estimates showed a steeper decline with age and were lower in non-Hispanic blacks.
CKD is common and warrants improved detection and classification using standardized criteria to improve outcomes. Am J Kidney Dis 41:1-12.
It has long been known that stratifying on variables affected by the study exposure can create selection bias. More recently it has been shown that stratifying on a variable that precedes exposure and disease can induce confounding, even if there is no confounding in the unstratified (crude) estimate. This paper examines the relative magnitudes of these biases under some simple causal models in which the stratification variable is graphically depicted as a collider (a variable directly affected by two or more other variables in the graph). The results suggest that bias from stratifying on variables affected by exposure and disease may often be comparable in size with bias from classical confounding (bias from failing to stratify on a common cause of exposure and disease), whereas other biases from collider stratification may tend to be much smaller.
There is a high prevalence of CVD in subjects with CKD. The presence of CKD, whether it is manifested by proteinuria (albuminuria) or reduced GFR, appears to be an independent risk factor for CVD outcomes, particularly in higher-risk populations. These findings are consistent with the NKF task force recommendation that patients with CKD should be considered in the highest-risk group for CVD events. The seventh report of the Joint National Committee for the Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC-7) includes CKD as a "compelling" indication, justifying lower target blood pressure and treatment with specific antihypertensive agents. Similarly, the recently published "NKF-K/DOQI Clinical Practice Guidelines on Managing Dyslipidemia in Chronic Kidney Disease" recommend that all patients with CKD be included in the highest-risk group, justifying a lower target low-density lipoprotein cholesterol level. By contrast, the third report of the Adult Treatment Panel of the National Cholesterol Education Program (ATP-III) does not include CKD in the list of high-risk conditions necessitating more aggressive management. We suggest that the National Cholesterol Education Program and other groups include CKD in the highest-risk group for recommendations for prevention, detection, and treatment of CVD risk factors. In addition, these findings reinforce the recent recommendation from the NKF on the importance of early identification and treatment of CKD and its associated comorbid conditions. We suggest that the routine evaluation of patients with CVD or those at high risk for CVD include measurement of spot urine albumin-to-creatinine ratio or total protein-to-creatinine ratio and estimation of GFR by serum creatinine and prediction equations. Finally, there is an urgent need for additional randomized controlled studies to evaluate potential treatments of CVD in CKD.
Air pollution is associated with stroke, and road traffic is a major source of outdoor air pollution. Using proximity to roads as a proxy for exposure to road traffic pollution, we examined the hypothesis that living near main roads increases the risk of stroke mortality.
We used a small-area ecological study design based on 113 465 census enumeration districts in England and Wales. Stroke mortality (International Classification of Disease, 9th revision, codes 430 through 438) in England and Wales from 1990 to 1992 for people >or=45 years of age was examined through the use of 1991 population denominators. Exposure was calculated as distance from each enumeration district population centroid to the nearest main road. We adjusted for age, sex, socioeconomic deprivation (using Carstairs index), regional variation, urbanization, and metropolitan area using Poisson regression.
The analysis was based on 189 966 stroke deaths and a population of 19 083 979. After adjustment for potential confounders, stroke mortality was 7% (95% confidence interval [CI], 4 to 9) higher in men living within 200 m of a main road compared with men living >or=1000 m away. The corresponding increase in risk for women was 4% (95% CI, 2 to 6) and the risk for men and women combined was 5% (95% CI, 4 to 7). These raised risks diminished with increasing distance from main roads.
Living near main roads is associated with excess risk of mortality from stroke, and if causality were assumed, approximately 990 stroke deaths per year would have been attributable to road traffic pollution.
End-stage renal disease substantially increases the risks of death, cardiovascular disease, and use of specialized health care, but the effects of less severe kidney dysfunction on these outcomes are less well defined.
We estimated the longitudinal glomerular filtration rate (GFR) among 1,120,295 adults within a large, integrated system of health care delivery in whom serum creatinine had been measured between 1996 and 2000 and who had not undergone dialysis or kidney transplantation. We examined the multivariable association between the estimated GFR and the risks of death, cardiovascular events, and hospitalization.
The median follow-up was 2.84 years, the mean age was 52 years, and 55 percent of the group were women. After adjustment, the risk of death increased as the GFR decreased below 60 ml per minute per 1.73 m2 of body-surface area: the adjusted hazard ratio for death was 1.2 with an estimated GFR of 45 to 59 ml per minute per 1.73 m2 (95 percent confidence interval, 1.1 to 1.2), 1.8 with an estimated GFR of 30 to 44 ml per minute per 1.73 m2 (95 percent confidence interval, 1.7 to 1.9), 3.2 with an estimated GFR of 15 to 29 ml per minute per 1.73 m2 (95 percent confidence interval, 3.1 to 3.4), and 5.9 with an estimated GFR of less than 15 ml per minute per 1.73 m2 (95 percent confidence interval, 5.4 to 6.5). The adjusted hazard ratio for cardiovascular events also increased inversely with the estimated GFR: 1.4 (95 percent confidence interval, 1.4 to 1.5), 2.0 (95 percent confidence interval, 1.9 to 2.1), 2.8 (95 percent confidence interval, 2.6 to 2.9), and 3.4 (95 percent confidence interval, 3.1 to 3.8), respectively. The adjusted risk of hospitalization with a reduced estimated GFR followed a similar pattern.
An independent, graded association was observed between a reduced estimated GFR and the risk of death, cardiovascular events, and hospitalization in a large, community-based population. These findings highlight the clinical and public health importance of chronic renal insufficiency.
Long-term exposure to fine-particulate-matter (PM2.5) air pollution may accelerate the development and progression of atherosclerosis. We investigated the associations of long-term residential exposure to traffic and fine particulate matter with the degree of coronary atherosclerosis.
We used baseline data on 4494 participants (age 45 to 74 years) from the German Heinz Nixdorf Recall Study, a population-based, prospective cohort study that started in 2000. To assess exposure differences, distances between residences and major roads were calculated, and annual fine particulate matter concentrations, derived from a small-scale dispersion model, were assigned to each address. The main outcome was coronary artery calcification (CAC) assessed by electron-beam computed tomography. We evaluated the association between air pollution and CAC with logistic and linear regression analyses, controlling for individual level risk factors of coronary atherosclerosis. Compared with participants living >200 m away from a major road, participants living within 50, 51 to 100, and 101 to 200 m had odds ratios of 1.63 (95% CI, 1.14 to 2.33), 1.34 (95% CI, 1.00 to 1.79), and 1.08 (95% CI, 0.85 to 1.39), respectively, for a high CAC (CAC above the age- and gender-specific 75th percentile). A reduction in the distance between the residence and a major road by half was associated with a 7.0% (95% CI, 0.1 to 14.4) higher CAC. Fine particulate matter exposure was associated with CAC only in subjects who had not been working full-time for at least 5 years.
Long-term residential exposure to high traffic is associated with the degree of coronary atherosclerosis.
Integrated science assessment for particulate matter (Final Report)
- U S Epa
U.S. EPA. Integrated Science Assessment for Particulate Matter (Final Report). Washington, DC:
U.S. Environmental Protection Agency; 2009.