Long-term Ambient Air Pollution Exposure Research Articles

Long-term ambient air pollution and coronary atherosclerosis: Results from the Swedish SCAPIS study

Background and aimsDespite firm evidence for an association between long-term ambient air pollution exposure and cardiovascular morbidity and mortality, results from epidemiological studies on the association between air pollution exposure and atherosclerosis have not been consistent. We investigated associations between long-term low-level air pollution exposure and coronary atherosclerosis. MethodsWe performed a cross-sectional analysis in the large Swedish CArdioPulmonary bioImaging Study (SCAPIS, n = 30 154), a random general population sample. Concentrations of total and locally emitted particulate matter <2.5 μm (PM2.5), <10 μm (PM10), and nitrogen oxides (NOx) at the residential address were modelled using high-resolution dispersion models. We estimated associations between air pollution exposures and segment involvement score (SIS), coronary artery calcification score (CACS), number of non-calcified plaques (NCP), and number of significant stenoses, using ordinal regression models extensively adjusted for potential confounders. ResultsMedian 10-year average PM2.5 exposure was 6.2 μg/m3 (range 3.5–13.4 μg/m3). 51 % of participants were women and 51 % were never-smokers. None of the assessed pollutants were associated with a higher SIS or CACS. Exposure to PM2.5 was associated with NCP (adjusted OR 1.34, 95 % CI 1.13, 1.58, per 2.05 μg/m3). Associations with significant stenoses were inconsistent. ConclusionsIn this large, middle-aged general population sample with low exposure levels, air pollution was not associated with measures of total burden of coronary atherosclerosis. However, PM2.5 appeared to be associated with a higher prevalence of non-calcified plaques. The results suggest that increased risk of early-stage atherosclerosis or rupture, but not increased total atherosclerotic burden, may be a pathway for long-term air pollution effects on cardiovascular disease.

The role of lifestyle in the association between long-term ambient air pollution exposure and cardiovascular disease: a national cohort study in China

BackgroundCardiovascular disease (CVD) caused by air pollution poses a considerable burden on public health. We aim to examine whether lifestyle factors mediate the associations of air pollutant exposure with the risk of CVD and the extent of the interaction between lifestyles and air pollutant exposure regarding CVD outcomes.MethodsWe included 7000 participants in 2011–2012 and followed up until 2018. The lifestyle evaluation consists of six factors as proxies, including blood pressure, blood glucose, blood lipids, body mass index, tobacco exposure, and physical activity, and the participants were categorized into three lifestyle groups according to the number of ideal factors (unfavorable, 0–1; intermediate, 2–4; and favorable, 5–6). Satellite-based spatiotemporal models were used to estimate exposure to ambient air pollutants (including particles with diameters ≤ 1.0 μm [PM1], ≤ 2.5 μm [PM2.5], ≤ 10 μm [PM10], nitrogen dioxide [NO2], and ozone [O3]). Cox regression models were used to examine the associations between air pollutant exposure, lifestyles and the risk of CVD. The mediation and modification effects of lifestyle categories on the association between air pollutant exposure and CVD were analyzed.ResultsAfter adjusting for covariates, per 10 μg/m3 increase in exposure to PM1 (HR: 1.09, 95% CI: 1.05–1.14), PM2.5 (HR: 1.04, 95% CI: 1.00–1.08), PM10 (HR: 1.05, 95% CI: 1.03–1.08), and NO2 (HR: 1.11, 95% CI: 1.05–1.18) was associated with an increased risk of CVD. Adherence to a healthy lifestyle was associated with a reduced risk of CVD compared to an unfavorable lifestyle (HR: 0.65, 95% CI: 0.56–0.76 for intermediate lifestyle and HR: 0.41, 95% CI: 0.32–0.53 for favorable lifestyle). Lifestyle played a significant partial mediating role in the contribution of air pollutant exposure to CVD, with the mediation proportion ranging from 7.4% for PM10 to 14.3% for PM2.5. Compared to an unfavorable lifestyle, the relative excess risk due to interaction for a healthier lifestyle to reduce the effect on CVD risk was − 0.98 (− 1.52 to − 0.44) for PM1, − 0.60 (− 1.05 to − 0.14) for PM2.5, − 1.84 (− 2.59 to − 1.09) for PM10, − 1.44 (− 2.10 to − 0.79) for NO2, and − 0.60 (− 1.08, − 0.12) for O3.ConclusionsLifestyle partially mediated the association of air pollution with CVD, and adherence to a healthy lifestyle could protect middle-aged and elderly people from the adverse effects of air pollution regarding CVD.

Long-term exposure to air pollution and incidence of gastric and the upper aerodigestive tract cancers in a pooled European cohort: The ELAPSE project.

Air pollution has been shown to significantly impact human health including cancer. Gastric and upper aerodigestive tract (UADT) cancers are common and increased risk has been associated with smoking and occupational exposures. However, the association with air pollution remains unclear. We pooled European subcohorts (N = 287,576 participants for gastric and N = 297,406 for UADT analyses) and investigated the association between residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone in the warm season (O3w) with gastric and UADT cancer. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. During 5,305,133 and 5,434,843 person-years, 872 gastric and 1139 UADT incident cancer cases were observed, respectively. For gastric cancer, we found no association with PM2.5, NO2 and BC while for UADT the hazard ratios (95% confidence interval) were 1.15 (95% CI: 1.00-1.33) per 5 μg/m3 increase in PM2.5, 1.19 (1.08-1.30) per 10 μg/m3 increase in NO2, 1.14 (1.04-1.26) per 0.5 × 10-5 m-1 increase in BC and 0.81 (0.72-0.92) per 10 μg/m3 increase in O3w. We found no association between long-term ambient air pollution exposure and incidence of gastric cancer, while for long-term exposure to PM2.5, NO2 and BC increased incidence of UADT cancer was observed.

Long-term ambient air pollution exposure and prospective change in sedentary behaviour and physical activity in individuals at risk of type 2 diabetes in the UK.

Air pollution may be a risk factor for physical inactivity and sedentary behaviour (SED) through discouraging active lifestyles, impairing fitness and contributing to chronic diseases with potentially important consequences for population health. Using generalized estimating equations, we examined the associations between long-term particulate matter with diameter≤2.5μm (PM2.5), ≤10μm (PM10) and nitrogen dioxide (NO2) and annual change in accelerometer-measured SED, moderate-to-vigorous physical activity (MVPA) and steps in adults at risk of type 2 diabetes within the Walking Away from Type 2 Diabetes trial. We adjusted for important confounders including social deprivation and measures of the built environment. From 808 participants, 644 had complete data (1605 observations; 64.7% men; mean age 63.86years). PM2.5, NO2 and PM10 were not associated with change in MVPA/steps but were associated with change in SED, with a 1ugm-3 increase associated with 6.38 (95% confidence interval: 0.77, 12.00), 1.52 (0.49, 2.54) and 4.48 (0.63, 8.34) adjusted annual change in daily minutes, respectively. Long-term PM2.5, NO2 and PM10 exposures were associated with an annual increase in SED: ~11-22min/day per year across the sample range of exposure (three standard deviations). Future research should investigate whether interventions to reduce pollution may influence SED.

Association of household solid fuel use and long-term exposure to ambient air pollution with estimated 10-year high cardiovascular disease risk among postmenopausal women

This study aimed to explore the separate and joint effects of long-term ambient air pollution and household air pollution exposure on 10-year high cardiovascular disease (CVD) risk among postmenopausal women. A total of 4679 postmenopausal women from the China Health and Retirement Longitudinal Study (CHARLS) were included in this study. Information of fuel type was collected by standard questionnaires and use of solid fuel was considered as a proxy for household air pollution. Data of ambient air pollutants (PM1, PM2.5, PM10, SO2, NO2, CO, O3) were obtained from the ChinaHighAirPollutants (CHAP) datasets. Logistic regression models were performed to assess the separate and joint effects of long-term exposure to ambient air pollution and use of solid fuel on 10-year high CVD risk. We found use of solid fuel and its duration and ambient air pollutants (PM1, PM2.5, PM10, SO2, NO2) were all positively associated with 10-year high CVD risk among postmenopausal women (P < 0.05). Compared to those used clean fuel and exposed to low ambient air pollution levels, odds ratios (ORs) and 95% confidence intervals (CIs) for participants using solid fuels and exposed to high ambient air pollution levels (PM1, PM2.5, PM10, SO2, NO2, CO, O3) were 1.66 (1.35, 2.05), 1.66 (1.35, 2.04), 1.49 (1.22, 1.83), 1.28 (1.05, 1.57), 1.67 (1.34, 2.07), 1.28 (1.04, 1.57), 1.46 (1.18, 1.80), respectively. Moreover, significant additive interactions of solid fuel use with PM1 and PM2.5 on 10-year high CVD risk were observed, with approximately 18% and 23% of 10-year high risk of CVD attributable to the interaction. Overall, indoor and outdoor air pollution had separate and joint effects on 10-year high CVD risk among postmenopausal women. Therefore, simultaneously improving indoor and outdoor air quality are of great importance and could have a joint impact on prevention of CVD and improved health among postmenopausal women.

Multiple myeloma risk in relation to long-term air pollution exposure - A pooled analysis of four European cohorts

BackgroundAir pollution is a growing concern worldwide, with significant impacts on human health. Multiple myeloma is a type of blood cancer with increasing incidence. Studies have linked air pollution exposure to various types of cancer, including leukemia and lymphoma, however, the relationship with multiple myeloma incidence has not been extensively investigated. MethodsWe pooled four European cohorts (N = 234,803) and assessed the association between residential exposure to nitrogen dioxide (NO2), fine particles (PM2.5), black carbon (BC), and ozone (O3) and multiple myeloma. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. ResultsDuring 4,415,817 person-years of follow-up (average 18.8 years), we observed 404 cases of multiple myeloma. The results of the fully adjusted linear analyses showed hazard ratios (95% confidence interval) of 0.99 (0.84, 1.16) per 10 μg/m³ NO2, 1.04 (0.82, 1.33) per 5 μg/m³ PM2.5, 0.99 (0.84, 1.18) per 0.5 10−5 m−1 BCE, and 1.11 (0.87, 1.41) per 10 μg/m³ O3. ConclusionsWe did not observe an association between long-term ambient air pollution exposure and incidence of multiple myeloma.

The association of long-term exposure to criteria air pollutants, fine particulate matter components, and airborne trace metals with late-life brain amyloid burden in the Atherosclerosis Risk in Communities (ARIC) study

BackgroundStudies suggest associations between long-term ambient air pollution exposure and outcomes related to Alzheimer’s disease (AD). Whether a link exists between pollutants and brain amyloid accumulation, a biomarker of AD, is unclear. We assessed whether long-term air pollutant exposures are associated with late-life brain amyloid deposition in Atherosclerosis Risk in Communities (ARIC) study participants. MethodsWe used a chemical transport model with data fusion to estimate ambient concentrations of PM2.5 and its components, NO2, NOx, O3 (24-hour and 8-hour), CO, and airborne trace metals. We linked concentrations to geocoded participant addresses and calculated 10-year mean exposures (2002 to 2011). Brain amyloid deposition was measured using florbetapir amyloid positron emission tomography (PET) scans in 346 participants without dementia in 2012–2014, and we defined amyloid positivity as a global cortical standardized uptake value ratio ≥ the sample median of 1.2. We used logistic regression models to quantify the association between amyloid positivity and each air pollutant, adjusting for putative confounders. In sensitivity analyses, we considered whether use of alternate air pollution estimation approaches impacted findings for PM2.5, NO2, NOx, and 24-hour O3. ResultsAt PET imaging, eligible participants (N = 318) had a mean age of 78 years, 56% were female, 43% were Black, and 27% had mild cognitive impairment. We did not find evidence of associations between long-term exposure to any pollutant and brain amyloid positivity in adjusted models. Findings were materially unchanged in sensitivity analyses using alternate air pollution estimation approaches for PM2.5, NO2, NOx, and 24-hour O3. ConclusionsAir pollution may impact cognition and dementia independent of amyloid accumulation, though whether air pollution influences AD pathogenesis later in the disease course or at higher exposure levels deserves further consideration.

Association of long-term air pollution and ambient noise with cognitive decline in the Heinz Nixdorf Recall study

Little is known about the impact of long-term ambient air pollution (AP) and noise exposure on change in cognitive function over years in the elderly. In this study, we wanted to examine the association between long-term exposure to AP and noise with the rate of cognitive decline in a population aged 50 and older and susceptible groups with mild cognitive impairment or at a genetically higher risk of Alzheimer's disease (Apolipoprotein E ε4 positive). Participants in the German population-based Heinz Nixdorf Recall study carried out five neuropsychological tests. Individual tests scores at the first (T1 = 2006–2008) and second (T2 = 2011–2015) follow-up for each test were used as outcomes after standardization using predicted means adjusted for age and education. Global cognitive score (GCS) was defined as sum of five standardized scores of individual tests. Long-term exposures to particulate matter (PM2.5, PM10, PM2.5 absorbance), accumulation mode particle number (PNacc), a proxy of ultrafine particles, and nitrogen dioxide were estimated by the land-use regression and chemistry transport models. Noise exposures were assessed as outdoor weighted nighttime road traffic noise (Lnight) means. We performed linear regression analyses adjusted for sex, age, individual and neighborhood socio-economic status, and lifestyle variables. Effect modification in vulnerable groups was estimated using multiplicative interaction terms between exposure and a modifier. Overall, 2554 participants (49.5% men, median age is 63 (IQR = 12)) were included. We found weak associations between higher exposure to PM10 and PM2.5 with faster decline in the immediate verbal memory test. Adjustment for potential confounders and for co-exposures did not change the results. We saw no effects on GCS, and no effect of noise exposure. In susceptible groups, higher AP and noise exposure were tended to be associated with faster decline in GCS. Our results suggest that AP exposure may accelerate cognitive decline in older ages, particularly in susceptible groups.

Long-term air pollution exposure and markers of cardiometabolic health in the National Longitudinal Study of Adolescent to Adult Health (Add Health)

BackgroundAir pollution exposure is associated with cardiovascular morbidity and mortality. Although exposure to air pollution early in life may represent a critical window for development of cardiovascular disease risk factors, few studies have examined associations of long-term air pollution exposure with markers of cardiovascular and metabolic health in young adults. ObjectivesBy combining health data from the National Longitudinal Study of Adolescent to Adult Health (Add Health) with air pollution data from the Fused Air Quality Surface using Downscaling (FAQSD) archive, we: (1) calculated multi-year estimates of exposure to ozone (O3) and particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM2.5) for Add Health participants; and (2) estimated associations between air pollution exposures and multiple markers of cardiometabolic health. MethodsAdd Health is a nationally representative longitudinal cohort study of over 20,000 adolescents aged 12–19 in the United States (US) in 1994–95 (Wave I). Participants have been followed through adolescence and into adulthood with five in-home interviews. Estimated daily concentrations of O3 and PM2.5 at census tracts were obtained from the FAQSD archive and used to generate tract-level annual averages of O3 and PM2.5 concentrations. We estimated associations between average O3 and PM2.5 exposures from 2002 to 2007 and markers of cardiometabolic health measured at Wave IV (2008–09), including hypertension, hyperlipidemia, body mass index (BMI), diabetes, C-reactive protein, and metabolic syndrome. ResultsThe final sample size was 11,259 individual participants. The average age of participants at Wave IV was 28.4 years (range: 24–34 years). In models adjusting for age, race/ethnicity, and sex, long-term O3 exposure (2002–07) was associated with elevated odds of hypertension, with an odds ratio (OR) of 1.015 (95% confidence interval [CI]: 1.011, 1.029); obesity (1.022 [1.004, 1.040]); diabetes (1.032 [1.009,1.054]); and metabolic syndrome (1.028 [1.014, 1.041]); PM2.5 exposure (2002–07) was associated with elevated odds of hypertension (1.022 [1.001, 1.045]). ConclusionFindings suggest that long-term ambient air pollution exposure, particularly O3 exposure, is associated with cardiometabolic health in early adulthood.

Long-term ambient air pollution exposure and cardio-respiratory disease in China: findings from a prospective cohort study

BackgroundExisting evidence on long-term ambient air pollution (AAP) exposure and risk of cardio-respiratory diseases in China is mainly on mortality, and based on area average concentrations from fixed-site monitors for individual exposures. Substantial uncertainty persists, therefore, about the shape and strength of the relationship when assessed using more personalised individual exposure data. We aimed to examine the relationships between AAP exposure and risk of cardio-respiratory diseases using predicted local levels of AAP.MethodsA prospective study included 50,407 participants aged 30–79 years from Suzhou, China, with concentrations of nitrogen dioxide (NO2), sulphur dioxide (SO2), fine (PM2.5), and inhalable (PM10) particulate matter, ozone (O3) and carbon monoxide (CO) and incident cases of cardiovascular disease (CVD) (n = 2,563) and respiratory disease (n = 1,764) recorded during 2013–2015. Cox regression models with time-dependent covariates were used to estimate adjusted hazard ratios (HRs) for diseases associated with local-level concentrations of AAP exposure, estimated using Bayesian spatio–temporal modelling.ResultsThe study period of 2013–2015 included a total of 135,199 person-years of follow-up for CVD. There was a positive association of AAP, particularly SO2 and O3, with risk of major cardiovascular and respiratory diseases. Each 10 µg/m3 increase in SO2 was associated with adjusted hazard ratios (HRs) of 1.07 (95% CI: 1.02, 1.12) for CVD, 1.25 (1.08, 1.44) for COPD and 1.12 (1.02, 1.23) for pneumonia. Similarly, each 10 µg/m3 increase in O3 was associated with adjusted HR of 1.02 (1.01, 1.03) for CVD, 1.03 (1.02, 1.05) for all stroke, and 1.04 (1.02, 1.06) for pneumonia.ConclusionsAmong adults in urban China, long-term exposure to ambient air pollution is associated with a higher risk of cardio-respiratory disease.

Effects of long-term ambient air pollution exposure on township-level pulmonary tuberculosis notification rates during 2005–2017 in Ningxia, China

Studies examining long-term effects of ambient air pollution exposure, measured as annual averages, on pulmonary tuberculosis (TB) incidence are scarce, particularly in endemic, rural settings. We performed a small-area study in Ningxia Hui Autonomous Region (NHAR), a high TB-burden area in rural China, using township-level (n = 358 non-overlapping townships) annual TB notification data (2005–2017). We aimed to determine if annual average concentrations of ambient air pollution (particulate matter <2·5 μm [PM2·5], nitrogen dioxide [NO2] ozone [O3]) were associated with TB notification rates (as a proxy for incidence). Air pollution effects on TB notification rates at township-level were estimated as incidence rate ratios (IRR), fitted using a generalised estimating equation (GEE) adjusted for covariates (age, sex, occupation, education, ethnicity, remoteness [urban or rural], household crowding and solid fuel use). A total of 38,942 TB notifications were reported in NHAR between 2005 and 2017. The mean annual TB notification rate was 67 (standard deviation [SD]; 7) per 100,000 people. Median concentrations of PM2·5, NO2, and O3 were 42 μg/m3 (interquartile range [IQR]; 38–48 μg/m3), 15 ppb (IQR; 12–16 ppb), and 56 ppb (IQR; 56–57 ppb), respectively. In single pollutant models, adjusted for covariates, an interquartile range (IQR) increase (10 μg/m3) in PM2·5 was significantly associated with higher TB notification rates (IRR: 1∙35; 95% CI: 1·25–1·48). Comparable effects on notifications of TB were observed for increases in NO2 exposure (IRR: 1·20 per IQR (4 ppb) increase; 95% CI: 1·08–1·31). Ground-level ozone was not associated with TB notification rate in any models. The observed effects were consistent over time, in multi-pollutant models, and appeared robust to additional adjustment for indicators of household crowding, solid fuel use and remoteness. More rigorous study designs are needed to understand if improving air quality has population-level benefits on TB disease incidence in endemic settings.

Long-term air pollution and risk of amyotrophic lateral sclerosis mortality in the Women's Health Initiative cohort

BackgroundAmyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder with no cure. Although the etiology of sporadic ALS is largely unknown, environmental exposures may affect ALS risk. ObjectiveWe investigated relationships between exposure to long-term ambient particulate matter (PM) and gaseous air pollution (AP) and ALS mortality. MethodsWithin the Women's Health Initiative (WHI) cohort of 161,808 postmenopausal women aged 50–79 years at baseline (1993–1998), we performed a nested case-control study of 256 ALS deaths and 2486 matched controls with emphasis on PM constituents (PM2.5, PM10, and coarse PM [PM10-2.5]) and gaseous pollutants (NOx, NO2, SO2, and ozone). Time-varying AP exposures estimates were averaged 5, 7.5, and 10 years prior to ALS death using both a GIS-based spatiotemporal generalized additive mixed model and ordinary kriging (empirical and multiple imputation, MI). Conditional logistic regression was used to estimate the relative risk of ALS death. ResultsIn general, PM2.5 and PM10-related risks were not significantly elevated using either method. However, for PM10-2.5, odds ratios (ORs) were >1.0 for both methods at all time periods using MI and empirical data for PM10-2.5 (coarse) except for 5 and 7.5 years using the kriging method with covariate adjustment. ConclusionThis investigation adds to the body of information on long-term ambient AP exposure and ALS mortality. Specifically, the 2019 US Environmental Protection Agency (EPA) Integrated Science Assessment summarized the neurotoxic effects of PM2.5, PM10, and PM10-2.5. The conclusion was that evidence of an effect of coarse PM is suggestive but the data is presently not sufficient to infer a causal relationship. Further research on AP and ALS is warranted. As time from symptom onset to death in ALS is ∼2–4 years, earlier AP measures may also be of interest to ALS development. This is the first study of ALS and AP in postmenopausal women controlling for individual-level confounders.

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

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

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

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

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

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

Long-term ambient air pollution exposure and tuberculosis notification rates during 2005–2017 in Ningxia Hui Autonomous Region, China

BACKGROUND AND AIM Pulmonary tuberculosis (TB) is a persistent public health concern, with 1.3 million attributable deaths and 10 million new cases recorded annually worldwide. Low- and middle-income countries account for the greatest proportion of TB cases globally (&amp;#x3e;95%), where some of the highest levels of air pollution occur. Epidemiological studies of an association, however, have been limited in number. We conducted a small-area study in Ningxia, a low socioeconomic and high TB-burden area in rural China, using TB-registry data (2005 – 2017). METHODS We used TB registry data to determine if annual average concentrations of remote-sensing based estimates of ambient air pollution (particulate matter &amp;#x3c;2.5 µm; [PM2.5], nitrogen dioxide [NO2] ozone [O3]) were associated with township-level (n=358) TB notification rates. Pollutant effects on age-standardised TB- notification rates (as Incidence Rate Ratios [IRR]) at township-level were estimated using Generalised Estimating Equations. RESULTS Median concentrations of PM2.5, NO2, and O3 were 42 µg/m3 (IQR: 10 µg/m3), 15 ppb (IQR: 4 ppb) and 56 ppb (IQR: 1 ppb), respectively. In single pollutant models adjusted for socio-economic covariates, an interquartile range (IQR) increase (10 µg/m3) in PM2.5 was significantly associated with an increase in TB notification incidence rates (IRR: 1.35; 95% CI: 1.27–1.41). Comparable effects were observed per IQR (4 ppb) increase in NO2 (IRR: 1.23; 95% CI: 1.19–1.28). Ground-level ozone was not associated with TB-notification rate in any models. The observed effects remained consistent in multi-pollutant models, and when adjusted for indicators of household crowding, solid fuel use and remoteness. CONCLUSIONS These findings may suggest that improving air quality may have population-level health benefits in socio-economically disadvantaged, TB-endemic settings. KEYWORDS Tuberculosis, TB, respiratory disease, China, outdoor air pollution

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

BACKGROUND AND AIM: Particulate matter (PM) is classified as a group 1 human carcinogen. Previous experimental studies suggest that particles in diesel exhaust induce oxidative stress, inflammation and DNA damage in kidney cells, but the evidence from population studies linking air pollution to kidney cancer is limited. METHODS: We included six cohorts from the &amp;#x22;Effects of low level air pollution: A study in Europe” (ELAPSE) collaboration. We developed hybrid models combining monitoring and land use data, satellite observations, and dispersion model estimates for nitrogen dioxide (NO2), fine PM (PM2.5), black carbon (BC), warm season ozone (O3), and eight elemental components of PM2.5 (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) to assign exposure to participants’ residential addresses. We defined kidney parenchyma cancer according to the International Classification of Diseases 10th and 9th Revision codes C64 and 189.0. We applied Cox proportional hazard models adjusting for potential confounders at the individual and area-level. RESULTS: A total of 302,493 persons were included in the analyses. During a total of 5,497,514 person-years of follow-up (mean 18.2 years), 847 incident cases of kidney parenchyma cancer occurred. Median (5–95%) exposure levels of NO2, PM2.5, BC and O3 were 24.1 µg/m3 (12.8–39.2), 15.3 µg/m3 (8.6–19.2), 1.6 10-5/m (0.7–2.1), and 87.0 µg/m3 (70.3–97.4), respectively. The results of the fully adjusted linear analyses showed a hazard ratio (95% confidence interval) of 1.03 (0.92, 1.15) per 10 &amp;#x3bc;g/m³ NO2, 1.04 (0.88, 1.21) per 5 &amp;#x3bc;g/m³ PM2.5, 0.99 (0.89, 1.11) per 0.5 10−5m−1 BC, and 0.88 (0.76, 1.02) per 10 &amp;#x3bc;g/m³ O3. The analyses did not show associations between any of the elemental components of PM2.5 and cancer of the kidney parenchyma. CONCLUSION: We did not observe evidence of an association between long-term ambient air pollution exposure and incidence of kidney parenchyma cancer.

Multi-pollutant air pollution and renal health in Asian children and adolescents: An 18-year longitudinal study

BackgroundFew 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. MethodsThis 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). ResultsMedian 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. ConclusionsLong-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.

Exposure to air pollution is associated with an increased risk of metabolic dysfunction-associated fatty liver disease

Accumulating animal studies have demonstrated the harmful contribution of ambient air pollution (AP) to metabolic dysfunction-associated fatty liver disease (MAFLD), but corresponding epidemiological evidence is limited. We examined the associations between long-term AP exposure and MAFLD prevalence in a Chinese population. We conducted a cross-sectional study of 90,086 participants recruited in China from 2018 to 2019. MAFLD was assessed based on radiologically diagnosed hepatic steatosis and the presence of overweight/obese status, diabetes mellitus, or metabolic dysregulation. Residence-specific levels of air pollutants, including particulate matter with aerodynamic diameters of ≤1 μm (PM1), ≤2.5 μm (PM2.5), and ≤10 μm (PM10), and nitrogen dioxide (NO2), were estimated by validated spatiotemporal models. We used logistic regression models to examine the AP-MAFLD associations and further evaluated potential effect modifications by demographics, lifestyle, central obesity, and diabetes status. Increased exposure levels to all 4 air pollutants were significantly associated with increased odds of MAFLD, with odds ratios (ORs) of 1.13 (95% CI 1.10-1.17), 1.29 (1.25-1.34), 1.11 (1.09-1.14), and 1.15 (1.12-1.17) for each 10 μg/m3 increase in PM1, PM2.5, PM10, and NO2, respectively. Further stratified analyses revealed that individuals who are male, alcohol drinkers, and current and previous smokers, those who consume a high-fat diet, and those with central obesity experience more significant adverse effects from AP exposure than other individuals. This study provides evidence that long-term exposure to ambient PM1, PM2.5, PM10, and NO2 may increase the odds of MAFLD in the real world. These effects may be exacerbated by unhealthy lifestyle habits and central obesity. We conducted an epidemiological study on the potential effect of ambient air pollution on the risk of metabolic dysfunction-associated fatty liver disease (MAFLD) in approximately 90 thousand adults in China. We found that long-term exposure to ambient air pollution may increase the odds of MAFLD, especially in individuals who are male, smokers, and alcohol drinkers, those who consume a high-fat diet, and those with central obesity.

Long-term air pollution and COVID-19 mortality rates in California: Findings from the Spring/Summer and Winter surges of COVID-19

A growing number of studies report associations between air pollution and COVID-19 mortality. Most were ecological studies at the county or regional level which disregard important local variability and relied on data from only the first few months of the pandemic. Using COVID-19 deaths identified from death certificates in California, we evaluated whether long-term ambient air pollution was related to weekly COVID-19 mortality at the census tract-level during the first ∼12 months of the pandemic. Weekly COVID-19 mortality for each census tract was calculated based on geocoded death certificate data. Annual average concentrations of ambient particulate matter <2.5 μm (PM2.5) and <10 μm (PM10), nitrogen dioxide (NO2), and ozone (O3) over 2014–2019 were assessed for all census tracts using inverse distance-squared weighting based on data from the ambient air quality monitoring system. Negative binomial mixed models related weekly census tract COVID-19 mortality counts to a natural cubic spline for calendar week. We included adjustments for potential confounders (census tract demographic and socioeconomic factors), random effects for census tract and county, and an offset for census tract population. Data were analyzed as two study periods: Spring/Summer (March 16-October 18, 2020) and Winter (October 19, 2020–March 7, 2021). Mean (standard deviation) concentrations were 10.3 (2.1) μg/m3 for PM2.5, 25.5 (7.1) μg/m3 for PM10, 11.3 (4.0) ppb for NO2, and 42.8 (6.9) ppb for O3. For Spring/Summer, adjusted rate ratios per standard deviation increase were 1.13 (95% confidence interval: 1.09, 1.17) for PM2.5, 1.16 (1.11, 1.21) for PM10, 1.06 (1.02, 1.10) for NO2, and 1.09 (1.04, 1.14) for O3. Associations were replicated in Winter, although they were attenuated for PM2.5 and PM10. Study findings support a relation between long-term ambient air pollution exposure and COVID-19 mortality. Communities with historically high pollution levels might be at higher risk of COVID-19 mortality.