Adjustment For PM2 Research Articles

Long-term exposure to road traffic noise and acute lower respiratory infections in the Danish Nurse Cohort

BackgroundLong-term exposure to road traffic noise is associated with cardiovascular disease, but the evidence on respiratory diseases is just emerging. We aimed to examine the association between long-term exposure to road traffic noise and the incidence of acute lower respiratory infections (ALRIs) in adults. MethodsWe followed 23,141 female nurses (age ≥ 44 years) from the Danish Nurse Cohort from baseline (1993 or 1999) to their first hospital contact (inpatient, outpatient, or emergency room) for ALRI, death, emigration or the end of 2015. The residential annual mean levels of road traffic noise (Lden) during the follow-up were estimated using the Nord2000 model. We applied time-varying Cox models to estimate the association of 3-year mean exposure to Lden with ALRIs incidence and piecewise analysis to estimate the threshold of Lden. We examined the robustness of the results by adjusting for residential exposure to air pollution, and the effect modification by attained age, socioeconomic status (SES), comorbidity, and lifestyle. ResultsDuring 18.5 years of follow-up, 2,004 nurses developed ALRIs. In a linear model, we detected a statistically significant positive association between Lden and ALRI, with a hazard ratio (HR) of 1.11 (95 % confidence interval (CI): 1.04, 1.17) per 9.2 dB (interquartile range, IQR). We observed non-linear association with a threshold at 57 dB, above which the HR was 1.25 (95 % CI: 1.09, 1.43) per IQR. Further adjustment for PM2.5 reduced the HRs slightly to 1.21 (95 % CI: 1.04, 1.40). The associations were stronger for nurses with asthma, and in those with lowest SES. ConclusionWe present novel findings in support of the association between long-term exposure to road traffic noise and ALRIs, independent of air pollution, suggesting noise as a risk factor for infectious respiratory diseases.

Long-term exposure to ozone and sleep disorders in children: A multicity study in China

Evidence regarding the link between long-term ambient ozone (O3) exposure and childhood sleep disorders is little. This study aims to examine the associations between long-term exposure to O3 and sleep disorders in children. We conducted a population-based cross-sectional survey, including 185,428 children aged 6–18 years in 173 schools across 14 Chinese cities during 2012 and 2018. Parents or guardians completed a checklist using Sleep Disturbance Scale for Children, and O3 exposure at residential and school addresses was estimated using a satellite-based spatiotemporal model. We used generalized linear mixed models to test the associations with adjustment for factors including socio-demographic variables, lifestyle, meteorology and multiple pollutants. Mean concentrations of O3, particulate matter with diameters ≤2.5 mm (PM2.5) and nitrogen dioxide (NO2) were 89.0 μg/m3, 42.5 μg/m3 and 34.4 μg/m3, respectively. O3 and NO2 concentrations were similar among provinces, while PM2.5 concentration varied significantly among provinces. Overall, 19.4% of children had at least one sleep disorder. Long-term exposure to O3 was positively associated with odds of sleep disorders for all subtypes. For example, each interquartile increment in home-school O3 concentrations was associated with a higher odds ratio for global sleep disorder, at 1.22 (95% confidence interval: 1.18, 1.26). Similar associations were observed for sleep disorder subtypes. The associations remained similar after adjustment for PM2.5 and NO2. Moreover, these associations were heterogeneous regionally, with more prominent associations among children residing in southeast region than in northeast and northwest regions in China. We concluded that long-term exposure to O3 is positively associated with risks of childhood sleep disorders. These associations varied by geographical region of China.

Source-Specific Air Pollution and Loss of Independence in Older Adults Across the US

Air pollution is a recognized risk factor associated with chronic diseases, including respiratory and cardiovascular conditions, which can lead to physical and cognitive impairments in later life. Although these losses of function, individually or in combination, reduce individuals' likelihood of living independently, little is known about the association of air pollution with this critical outcome. To investigate associations between air pollution and loss of independence in later life. This cohort study was conducted as part of the Environmental Predictors Of Cognitive Health and Aging study and used 1998 to 2016 data from the Health and Retirement Study. Participants included respondents from this nationally representative, population-based cohort who were older than 50 years and had not previously reported a loss of independence. Analyses were performed from August 31 to October 15, 2023. Mean 10-year pollutant concentrations (particulate matter less than 2.5 μm in diameter [PM2.5] or ranging from 2.5 μm to 10 μm in diameter [PM10-2.5], nitrogen dioxide [NO2], and ozone [O3]) were estimated at respondent addresses using spatiotemporal models along with PM2.5 levels from 9 emission sources. Loss of independence was defined as newly receiving care for at least 1 activity of daily living or instrumental activity of daily living due to health and memory problems or moving to a nursing home. Associations were estimated with generalized estimating equation regression adjusting for potential confounders. Among 25 314 respondents older than 50 years (mean [SD] baseline age, 61.1 [9.4] years; 11 208 male [44.3%]), 9985 individuals (39.4%) experienced lost independence during a mean (SD) follow-up of 10.2 (5.5) years. Higher exposure levels of mean concentration were associated with increased risks of lost independence for total PM2.5 levels (risk ratio [RR] per 1-IQR of 10-year mean, 1.05; 95% CI, 1.01-1.10), PM2.5 levels from road traffic (RR per 1-IQR of 10-year mean, 1.09; 95% CI, 1.03-1.16) and nonroad traffic (RR per 1-IQR of 10-year mean, 1.13; 95% CI, 1.03-1.24), and NO2 levels (RR per 1-IQR of 10-year mean, 1.05; 95% CI, 1.01-1.08). Compared with other sources, traffic-generated pollutants were most consistently and robustly associated with loss of independence; only road traffic-related PM2.5 levels remained associated with increased risk after adjustment for PM2.5 from other sources (RR per 1-IQR increase in 10-year mean concentration, 1.10; 95% CI, 1.00-1.21). Other pollutant-outcome associations were null, except for O3 levels, which were associated with lower risks of lost independence (RR per 1-IQR increase in 10-year mean concentration, 0.94; 95% CI, 0.92-0.97). This study found that long-term exposure to air pollution was associated with the need for help for lost independence in later life, with especially large and consistent increases in risk for pollution generated by traffic-related sources. These findings suggest that controlling air pollution could be associated with diversion or delay of the need for care and prolonged ability to live independently.

Ambient air pollution and hypertensive disorders of pregnancy in Rome

BackgroundAmbient air pollution has been associated with hypertensive disorders of pregnancy (HDP), but few studies rely on assessment of fine-scale variation in air quality, specific subtypes and multi-pollutant exposures. AimTo study the impact of long-term exposure to individual and mixture of air pollutants on all and specific subtypes of HDP. MethodsWe obtained data from 130,470 liveborn singleton pregnacies in Rome during 2014–2019. Spatiotemporal land-use random-forest models at 1 km spatial resolution assigned to the maternal residential addresses were used to estimate the exposure to particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2), and ozone (O3). ResultsFor PM2.5, PM10 and NO2, there was suggestive evidence of increased risk of preeclampsia (PE, n = 442), but no evidence of increased risk for all subtypes of HDP (n = 2297) and gestational hypertension (GH, n = 1901). For instance, an interquartile range of 7.0 μg/m3 increase in PM2.5 exposure during the first trimester of pregnancy was associated with an odds ratio (OR) of 1.06 (95% confidence interval: 0.81, 1.39) and 1.04 (0.92, 1.17) after adjustment for NO2 and the corresponding results for a 15.7 μg/m3 increase in NO2 after adjustment for PM2.5 were 1.11 (0.92, 1.34) for PE and 0.83 (0.76, 0.90) for HDP. Increased risks for HDP and GH were suggested for O3 in single-pollutant models and for PM after adjustment for NO2, but all other associations were stable or attenuated in two-pollutant models. ConclusionsThe results of our study suggest that PM2.5, PM10 and NO2 increases the risk of PE and that these effects are robust to adjustment for O3 while the increased risks for GH and HDP suggested for O3 attenuated after adjustment for PM or NO2. Additional studies are needed to evaluate the effects of source-specific component of PM on subtypes as well as all types of HDP which would help to target preventive actions.

Outdoor light at night and mortality in the UK Biobank: a prospective cohort study

BackgroundMore than 83% of the world’s population lives under light-polluted skies while information about health effects of outdoor light at night (LAN) is limited. We examined the association of LAN...

Exposure to long-term source-specific transportation noise and incident breast cancer: A pooled study of eight Nordic cohorts

BackgroundEnvironmental noise is an important environmental exposure that can affect health. An association between transportation noise and breast cancer incidence has been suggested, although current evidence is limited. We investigated the pooled association between long-term exposure to transportation noise and breast cancer incidence. MethodsPooled data from eight Nordic cohorts provided a study population of 111,492 women. Road, railway, and aircraft noise were modelled at residential addresses. Breast cancer incidence (all, estrogen receptor (ER) positive, and ER negative) was derived from cancer registries. Hazard ratios (HR) were estimated using Cox Proportional Hazards Models, adjusting main models for sociodemographic and lifestyle variables together with long-term exposure to air pollution. ResultsA total of 93,859 women were included in the analyses, of whom 5,875 developed breast cancer. The median (5th–95th percentile) 5-year residential road traffic noise was 54.8 (40.0–67.8) dB Lden, and among those exposed, the median railway noise was 51.0 (41.2–65.8) dB Lden. We observed a pooled HR for breast cancer (95 % confidence interval (CI)) of 1.03 (0.99–1.06) per 10 dB increase in 5-year mean exposure to road traffic noise, and 1.03 (95 % CI: 0.96–1.11) for railway noise, after adjustment for lifestyle and sociodemographic covariates. HRs remained unchanged in analyses with further adjustment for PM2.5 and attenuated when adjusted for NO2 (HRs from 1.02 to 1.01), in analyses using the same sample. For aircraft noise, no association was observed. The associations did not vary by ER status for any noise source. In analyses using <60 dB as a cutoff, we found HRs of 1.08 (0.99–1.18) for road traffic and 1.19 (0.95–1.49) for railway noise. ConclusionsWe found weak associations between road and railway noise and breast cancer risk. More high-quality prospective studies are needed, particularly among those exposed to railway and aircraft noise before conclusions regarding noise as a risk factor for breast cancer can be made.

Residential greenness, air pollution and incident neurodegenerative disease: A cohort study in China

BackgroundNeurodegenerative disease has a great adverse impact on population's death and disability worldwide. However, the association of air pollution and residential greenness with neurodegenerative disease and their potential mechanisms still remain uncertain. MethodsWe used data from a population-based prospective cohort in Ningbo, China. Exposure to PM2.5, PM10 and NO2 were assessed by land-use regression (LUR) models and residential greenness was estimated by Normalized Difference Vegetation Index (NDVI). Our primary outcomes were all neurodegenerative diseases, Parkinson's disease (PD) and Alzheimer's disease (AD). Cox proportional hazards regression models were used to examine the association of air pollution and residential greenness with risk of incident neurodegenerative disease. Furthermore, we also explored the potential mediation relationship and effect modification between greenness and air pollutants. ResultsDuring the follow-up period, we identified a total of 617 incident neurodegenerative diseases, 301 PD and 182 AD. In single-exposure models, PM2.5 was positively associated with all outcomes (e.g. AD hazard ratio (HR): 1.41, 95 % confidence interval (CI): 1.09–1.84, per interquartile range (IQR) increment), whereas residential greenness showed protective effects (e.g. neurodegenerative disease, HR: 0.82, 95%CI: 0.75–0.90, per IQR increment for NDVI in 1000 m buffer). NO2 was positively associated with risk of neurodegenerative disease and PM10 was associated with neurodegenerative disease and AD. In two-exposure models, after adjustment for PM2.5, the association for greenness generally attenuated towards null. Moreover, we identified the significant modification effect of greenness on PM2.5 on additive and multiplicative scales. ConclusionIn this prospective study, we found that exposure to higher residential greenness and lower concentrations of particulate matter were associated with lower risk of neurodegenerative disease, PD and AD. Residential greenness could modify the association of PM2.5 with neurodegenerative disease.

Ambient temperature and air pollution associations with suicide and homicide mortality in California: A statewide case-crossover study

BackgroundHigher ambient temperature and air pollution may contribute to increased risk of behaviors harmful to oneself or to others; however, quantitative evidence is limited. We examined the relationship of deaths due to suicide and homicide with temperature and air pollution in California—a state prone to high levels of both exposures. MethodCalifornia death certificates from 2014 to 2019 were used to identify deaths due to suicide and homicide. Residential data for decedents were used to assign exposure to daily temperature (maximum[Tmax], minimum[Tmin]) and daily average air pollution concentrations (particulate matter <10 μm[PM10] and < 2.5 μm[PM2.5], nitrogen dioxide[NO2], ozone[O3]). Tmin served as a surrogate for nighttime temperature. A time-stratified case-crossover study design using conditional logistic regression was used to assess the effects of daily exposure to temperature and air pollutants on suicide and homicide mortality, adjusting for relative humidity. Effect modification by sex and age was assessed. ResultsWe observed 24,387 deaths due to suicide and 10,767 deaths due to homicide. We found a monotonic temperature association for both outcomes. A 5 °C increase in Tmax at lag-2 and Tmin at lag-0 was associated with 3.1 % (95 % confidence interval [CI]: 1.1 %–5.2 %) and 3.8 % (95%CI: 0.9 %–6.8 %) increased odds of death due to suicide, respectively. The increased odds of homicide mortality per 5 °C increase in Tmax at lag-0 and Tmin at lag-1 were 4.9 % (95%CI: 1.6 %–8.1 %) and 6.2 % (95%CI: 1.6 %–11.0 %), respectively. No air pollutant associations were statistically significant. Temperature associations were robust after adjustment for PM2.5. Some temperature effects were larger among women for suicide and men for homicide mortality, and among those over age 65 years for both outcomes. ConclusionRisk of suicide and homicide mortality increases with increasing daily ambient temperatures. Findings have public health relevance given anticipated increases in temperatures due to global climate change.

Associations of road traffic noise and its frequency spectrum with prevalent depression in Taichung, Taiwan.

Exposure to road traffic noise has been reported to be associated with depression in many epidemiological studies, but the association between noise frequency spectrum and depression remains unclear. This community-based study investigated the associations between road traffic noise exposure and its frequency components with prevalent depression. A total of 3,191 residents living in Taichung who participated in the Taiwan Biobank between 2010 and 2017, were included as study participants. The land-use regression models were used to evaluate individual annual average values of A-weighted equivalent sound level over 24 h (Leq,24h) and particulate matter with an aerodynamic diameter <2.5 μm (PM2.5) using the geographic information system. Multiple logistic regression was applied to estimate the odds ratios (ORs) for depression after adjusting for potential risk factors and PM2.5. An interquartile range increase in Leq,24h at full frequency (4.7 dBA), 1,000 Hz (5.2 dB), and 2,000 Hz (4.8 dB) was significantly associated with an elevated risk for depression with ORs of 1.62 (95% confidence interval [CI]: 1.03, 2.55), 1.58 (95% CI: 1.05, 2.37), and 1.58 (95% CI:1.03, 2.43), respectively, by controlling for PM2.5. The high-exposure group (≥3rd quartile median of noise levels) at full frequency, 1,000 Hz, and 2,000 Hz had an increased risk for depression with ORs of 2.65 (95% CI: 1.16-6.05), 2.47 (95% CI: 1.07-5.70), and 2.60 (95% CI: 1.10-6.12), respectively, compared with the reference group (<1st quartile of noise levels) after adjustment for PM2.5. Significant exposure-response trends were observed between the prevalent depression and noise exposure by quartiles at full frequency, 1,000 Hz, and 2,000 Hz (all p < 0.05). Exposure to road traffic noise may be associated with an increased prevalence of depression, particularly at 1,000 and 2,000 Hz.

Epigenome-wide analysis of maternal exposure to green space during gestation and cord blood DNA methylation in the ENVIRONAGE cohort

BackgroundDNA methylation programming is sensitive to prenatal life environmental influences, but the impact of maternal exposure to green space on newborns DNA methylation has not been studied yet. MethodsWe conducted a meta-epigenome-wide association study (EWAS) of maternal exposure to green space during gestation with cord blood DNA methylation in two subsets of the ENVIRONAGE cohort (N = 538). Cord blood DNA methylation was measured by Illumina HumanMethylation 450K in one subset (N = 189) and EPICarray in another (N = 349). High (vegetation height>3 m (m)), low (vegetation height<3 m) and total (including both) high-resolution green space exposures during pregnancy were estimated within 100 m and 1000 m distance around maternal residence. In each subset, we sought cytosine-phosphate-guanine (CpG) sites via linear mixed models adjusted on newborns' sex, ethnicity, gestational age, season at delivery, sampling day, maternal parity, age, smoking, education, and estimated blood cell proportions. EWASs results were meta-analysed via fixed-effects meta-analyses. Differentially methylated regions (DMRs) were identified via ENmix-combp and DMRcate algorithms. Sensitivity analyses were additionally adjusted on PM2.5, distance to major roads, urbanicity and neighborhood income. In the 450K subset, cord blood expression of differentially methylated genes was measured by Agilent microarrays and associated with green space. Results147 DMRs were identified, 85 of which were still significant upon adjustment for PM2.5, distance to major roads, urbanicity and neighborhood income, including HLA-DRB5, RPTOR, KCNQ1DN, A1BG-AS1, HTR2A, ZNF274, COL11A1 and PRSS36 DMRs. One CpG reached genome-wide significance, while 54 CpGs were suggestive significant (p-values<1e-05). Among them, a CpG, hypermethylated with 100 m buffer total green space, was annotated to PAQR9, whose expression decreased with 1000 m buffer low green space (p-value = 1.45e-05). ConclusionsOur results demonstrate that maternal exposure to green space during pregnancy is associated with cord blood DNA methylation, mainly at loci organized in regions, in genes playing important roles in neurological development (e.g., HTR2A).

Long-term exposure to transportation noise and risk of type 2 diabetes: a cohort study

BACKGROUND AND AIM A few studies have reported associations between transportation noise and diabetes. This includes studies based on millions of participants, relying entirely on register-based confounder adjustment, which raises concern about residual confounding from lifestyle. We aimed to investigate associations between road and railway noise and risk of type 2 diabetes (T2D), including investigation of effects of increasing adjustment for register-based and lifestyle covariates. METHODS In a population-based cohort of 324,988 participants randomly selected across Denmark in 2010–2013 and followed up until December 2017, we identified 7,574 incident T2D cases using hospital and prescription registries. Based on historical address-information, we calculated 10-year time-weighted exposure to road noise at the most (LdenMax) and least (LdenMin) exposed façades and exposure to air pollution (PM2.5). We used Cox proportional hazards models to calculate hazard ratios (HR) with increasing adjustment for individual- and area-level register-based sociodemographic covariates (e.g. education and income) and lifestyle covariates assessed through questionnaires, including smoking, physical activity and alcohol. RESULTS We found that a 10 dB increase in road LdenMin was associated with HRs (95% CI) of 1.06 (1.02–1.10) in the crude model, 1.08 (1.04–1.13) after adjustment for register-based sociodemographic covariates and 1.07 (1.03–1.12) after further adjustment for lifestyle. For road LdenMax, the corresponding HRs were 1.07 (1.04–1.10), 1.05 (1.02–1.08) and 1.04 (1.01–1.07). After further adjustment for PM2.5, HRs were 1.06 (1.01–1.10) for LdenMin and 1.03 (1.00–1.07) for LdenMax. Railway noise was associated with HRs of 1.05 (0.98–1.11) for LdenMax and 1.04 (0.94–1.14) for LdenMin in fully adjusted models. CONCLUSIONS Long-term exposure to road and potentially railway noise was associated with T2D. Our results indicated that administrative cohort studies can produce reliable results if a broad register-based adjustment strategy is applied. KEYWORDS Road noise; railway noise; type 2 diabetes; lifestyle

Association of sound pressure levels and frequency components of road traffic noise with prevalent depression in Taichung, Taiwan

The World Health Organization has reported that the prevalence of mental illness is 4% in the global population. Epidemiological studies have reported a relationship between road traffic noise exposure and depression, but the association between noise frequency components and depression remains unclear. This cross-sectional study investigated the associations between road traffic noise exposure and its frequency components with prevalent depression. A total of 3,200 residents living in Taichung who participated in the Taiwan Biobank between 2010 and 2017, were included as study participants. We used land-use regression models to evaluate individual annual average values of A-weighted equivalent sound level over 24 h (Leq,24h) and particulate matter with an aerodynamic diameter less than 2.5 &amp;#x3bc;m (PM2.5) using the geographic information system. Multiple logistic regression was applied to estimate the odds ratios (ORs) for depression after adjusting for potential risk factors and PM2.5. An interquartile range increase in Leq,24h at full frequency (4.7 dBA), 1000 Hz (5.2 dB), and 2000 Hz (4.8 dB) was significantly associated with an elevated risk for depression with ORs of 1.62 (95% confidence interval [CI]: 1.03, 2.55), 1.58 (95% CI: 1.05, 2.37), and 1.58 (95% CI:1.03, 2.43), respectively, by controlling for PM2.5. The high-exposure group (&amp;#x2265; the median of noise levels) at full frequency, 500 Hz, and 2000 Hz had an increased risk for depression with ORs of 1.87 (95% CI: 1.03, 3.39), 1.94 (95% CI: 1.03, 3.65), and 1.86 (95% CI: 1.03, 3.37), respectively, compared with the low-exposure group (&amp;#x3c; the median of noise levels) after adjustment for PM2.5. Road traffic noise exposure may be associated with an increased prevalence of depression, particularly at 500 to 2000 Hz.

Air pollution enhance the progression of restrictive lung function impairment and diffusion capacity reduction: an elderly cohort study

BackgroundSome evidences have shown the association between air pollution exposure and the development of interstitial lung diseases. However, the effect of air pollution on the progression of restrictive ventilatory impairment and diffusion capacity reduction is unknown. This study aimed to evaluate the effects of long-term exposure to ambient air pollution on the change rates of total lung capacity, residual volume, and diffusion capacity among the elderly.MethodsFrom 2016 to 2018, single-breath helium dilution with the diffusion capacity of carbon monoxide was performed once per year on 543 elderly individuals. Monthly concentrations of ambient fine particulate matters (PM2.5) and nitric dioxide (NO2) at the individual residential address were estimated using a hybrid Kriging/Land-use regression model. Linear mixed models were used to evaluate the association between long-term (12 months) exposure to air pollution and lung function with adjustment for potential covariates, including basic characteristics, indoor air pollution (second-hand smoke, cooking fume, and incense burning), physician diagnosed diseases (asthma and chronic airway diseases), dusty job history, and short-term (lag one month) air pollution exposure.ResultsAn interquartile range (5.37 ppb) increase in long-term exposure to NO2 was associated with an additional rate of decline in total lung volume (− 1.8% per year, 95% CI: − 2.8 to − 0.9%), residual volume (− 3.3% per year, 95% CI: − 5.0 to − 1.6%), ratio of residual volume to total lung volume (− 1.6% per year, 95% CI: − 2.6 to − 0.5%), and diffusion capacity (− 1.1% per year, 95% CI: − 2.0 to − 0.2%). There is no effect on the transfer factor (ratio of diffusion capacity to alveolar volume). The effect of NO2 remained robust after adjustment for PM2.5 exposure.ConclusionsLong-term exposure to ambient NO2 is associated with an accelerated decline in static lung volume and diffusion capacity in the elderly. NO2 related air pollution may be a risk factor for restrictive lung disorders.

Acute effects of ambient non-methane hydrocarbons on cardiorespiratory hospitalizations: A multicity time-series study in Taiwan

BackgroundFew environmental epidemiological studies and no large multicity studies have evaluated the acute short-term health effects of ambient non-methane hydrocarbons (NMHC), the essential precursors of ground-level ozone and secondary organic aerosol formation. ObjectiveWe conducted this multicity time-series study in Taiwan to evaluate the association between airborne NMHC exposure and cardiorespiratory hospital admissions. MethodsWe collected the daily mean concentrations of NMHC, fine particulate matter (PM2.5), ozone (O3), weather conditions, and daily hospital admission count for cardiorespiratory diseases between 2014 and 2017 from eight major cities of Taiwan. We applied an over-dispersed generalized additive Poisson model (GAM) with adjustment for temporal trends, seasonal variations, weather conditions, and calendar effects to compute the effect estimate for each city. Then we conducted a random-effects meta-analysis to pool the eight city-specific effect estimates to obtain the overall associations of NMHC exposure on lag0 day with hospital admissions for respiratory and circulatory diseases, respectively. ResultsOn average, a 0.1-ppm increase of lag0 NMHC demonstrated an overall 0.9% (95% CI: 0.4–1.3%) and 0.8% (95% CI: 0.4–1.2%) increment of hospital admissions for respiratory and circulatory diseases, respectively. Further analyses with adjustment for PM2.5 and O3 in the multi-pollutant model or sensitivity analyses with restricting the NMHC monitoring from the general stations only confirmed the robustness of the association between ambient NMHC exposure and cardiorespiratory hospitalizations. ConclusionOur findings provide robust evidence of higher cardiorespiratory hospitalizations in association with acute exposure to ambient NMHC in eight major cities of Taiwan.

Does apparent temperature modify the effects of air pollution on respiratory disease hospital admissions in an industrial area of South Africa?

Background: Temperature and air pollution are often treated as separate risk factors and very few studies have investigated effect modification by temperature on air pollution, and the impact of this interaction on human health in Africa. This study therefore investigated the modifying effects of temperature on the association between air pollution and Respiratory disease (RD) hospital admission in South Africa.&#x0D; Methods: RD admission data (ICD10 J00-J99) were obtained from two hospitals located in Secunda, South Africa beween 1 January 2011 to 31 October 2016. NO2, SO2, PM10, PM2.5, temperature and relative humidity data were obtained from the South African Weather Services. A case-crossover epidemiological study design was applied and lag0-1 was used. Models were adjusted for public holidays and Apparent Temperature (Tapp). Tapp was classified as warm (Tapp&gt;75th percentile), cold (Tapp&lt;25th percentile) and normal (Tapp 25th-75th percentile).&#x0D; Results: Of the 14 568 RD admissions, approximately equal number of females and males were admitted. The average daily NO2, SO2, PM2.5 and PM10 levels were 12.4 μm/m3, 8.5 μm/m3, 32.3 μm/m3 and 68.6 μm/m3, respectively. Overall, a 10 μm/m3 increase in SO2 on warm days was associated with an increase in RD hospital admissions among the patients by 8.5% (95% Conf. Int: 0.4%, 17.2%) and 8.4% (95% Conf. Int: 0.3%, 17.1%) after adjustment for PM2.5 and PM10 respectively. However, increasing PM2.5 or PM10 by 10 μm/m3 was associated with an increase in RD hospital admissions when the temperature was normal after adjusting for SO2. On cold days there were significant associations between the SO2 and RD admissions among the 0-14 year age group after adjusting for either PM2.5 (6.5%; 95% Conf.Int: 0.9%, 12.4%) or PM10 (5.5%; 95% Conf.Int: 0.3%, 11.1%).&#x0D; Conclusions: SO2 was affected by extremes of temperature while the particulate matters had effect on RD admission during normal temperature in Secunda.

Long-term exposure to transportation noise and risk for atrial fibrillation: A Danish nationwide cohort study

Epidemiological studies have linked transportation noise and cardiovascular diseases, however, atrial fibrillation (AF) has received limited attention. We aimed to investigate the association between transportation noise and AF risk. Over the period 1990-2017 we estimated road and railway noise (Lden) at the most and least exposed façades for all residential addresses across Denmark. We estimated time-weighted mean noise exposure for 3.6 million individuals age ≥35 years. Of these, 269,756 incident cases of AF were identified with a mean follow-up of 13.0 years. Analyses were conducted using Cox proportional hazards models with adjustment for individual and area-level sociodemographic covariates and long-term residential air pollution. A 10dB higher 10-year mean road traffic noise at the most and least exposed façades were associated with incidence rate ratios (IRR) and 95% confidence intervals (CI) for AF of 1.006 (1.001-1.011) and 1.013 (1.007-1.019), respectively. After further adjustment for PM2.5, the IRRs (CIs) were 1.000 (0.995-1.005) and 1.007 (1.000-1.013), respectively. For railway noise, the IRRs per 10dB increase in 10-year mean exposure were 1.017 (1.007-1.026) and 1.035 (1.021-1.050) for the most and least exposed façades, respectively, and were slightly attenuated when adjusted for PM2.5. Aircraft noise between 55 and 60dB and ≥60dB were associated with IRRs of 1.055 (0.996-1.116) and 1.036 (0.931-1.154), respectively, when compared to <45dB. Transportation noise seems to be associated with a small increase in AF risk, especially for exposure at the least exposed façade.

A Population-Based Cohort Study of Respiratory Disease and Long-Term Exposure to Iron and Copper in Fine Particulate Air Pollution and Their Combined Impact on Reactive Oxygen Species Generation in Human Lungs.

Metal components in fine particulate matter (PM2.5) from nontailpipe emissions may play an important role in underlying the adverse respiratory effects of PM2.5. We investigated the associations between long-term exposure to iron (Fe) and copper (Cu) in PM2.5 and their combined impact on reactive oxygen species (ROS) generation in human lungs, and the incidence of asthma, chronic obstructive pulmonary disease (COPD), COPD mortality, pneumonia mortality, and respiratory mortality. We conducted a population-based cohort study of ∼0.8 million adults in Toronto, Canada. Land-use regression models were used to estimate the concentrations of Fe, Cu, and ROS. Outcomes were ascertained using validated health administrative databases. We found positive associations between long-term exposure to Fe, Cu, and ROS and the risks of all five respiratory outcomes. The associations were more robust for COPD, pneumonia mortality, and respiratory mortality than for asthma incidence and COPD mortality. Stronger associations were observed for ROS than for either Fe or Cu. In two-pollutant models, adjustment for nitrogen dioxide somewhat attenuated the associations while adjustment for PM2.5 had little influence. Long-term exposure to Fe and Cu in PM2.5 and estimated ROS concentration in lung fluid was associated with increased incidence of respiratory diseases, suggesting the adverse respiratory effects of nontailpipe emissions.

Long-term exposure to iron and copper in fine particulate air pollution and their combined impact on reactive oxygen species concentration in lung fluid: a population-based cohort study of cardiovascular disease incidence and mortality in Toronto, Canada.

Exposure to fine particulate (PM2.5) air pollution is associated with increased cardiovascular disease (CVD), but less is known about its specific components, such as metals originating from non-tailpipe emissions. We investigated the associations of long-term exposure to metal components [iron (Fe) and copper (Cu)] in PM2.5 with CVD incidence. We conducted a population-based cohort study in Toronto, Canada. Exposures to Fe and Cu in PM2.5 and their combined impact on the concentration of reactive oxygen species (ROS) in lung fluid were estimated using land use regression models. Incidence of acute myocardial infarction (AMI), congestive heart failure (CHF) and CVD death was ascertained using health administrative datasets. We used mixed-effects Cox regression models to examine the associations between the exposures and health outcomes. A series of sensitivity analyses were conducted, including indirect adjustment for individual-level cardiovascular risk factors (e.g. smoking), and adjustment for PM2.5 and nitrogen dioxide (NO2). In single-pollutant models, we found positive associations between the three exposures and all three outcomes, with the strongest associations detected for the estimated ROS. The associations of AMI and CHF were sensitive to indirect adjustment, but remained robust for CVD death in all sensitivity analyses. In multi-pollutant models, the associations of the three exposures generally remained unaltered. Interestingly, adjustment for ROS did not substantially change the associations between PM2.5 and CVD, but attenuated the associations of NO2. Long-term exposure to Fe and Cu in PM2.5 and their combined impact on ROS were consistently associated with increased CVD death.

Long-term exposure to fine particle elemental components and lung cancer incidence in the ELAPSE pooled cohort

BackgroundAn association between long-term exposure to fine particulate matter (PM2.5) and lung cancer has been established in previous studies. PM2.5 is a complex mixture of chemical components from various sources and little is known about whether certain components contribute specifically to the associated lung cancer risk. The present study builds on recent findings from the “Effects of Low-level Air Pollution: A Study in Europe” (ELAPSE) collaboration and addresses the potential association between specific elemental components of PM2.5 and lung cancer incidence. MethodsWe pooled seven cohorts from across Europe and assigned exposure estimates for eight components of PM2.5 representing non-tail pipe emissions (copper (Cu), iron (Fe), and zinc (Zn)), long-range transport (sulfur (S)), oil burning/industry emissions (nickel (Ni), vanadium (V)), crustal material (silicon (Si)), and biomass burning (potassium (K)) to cohort participants’ baseline residential address based on 100 m by 100 m grids from newly developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status). ResultsThe pooled study population comprised 306,550 individuals with 3916 incident lung cancer events during 5,541,672 person-years of follow-up. We observed a positive association between exposure to all eight components and lung cancer incidence, with adjusted HRs of 1.10 (95% CI 1.05, 1.16) per 50 ng/m3 PM2.5 K, 1.09 (95% CI 1.02, 1.15) per 1 ng/m3 PM2.5 Ni, 1.22 (95% CI 1.11, 1.35) per 200 ng/m3 PM2.5 S, and 1.07 (95% CI 1.02, 1.12) per 200 ng/m3 PM2.5 V. Effect estimates were largely unaffected by adjustment for nitrogen dioxide (NO2). After adjustment for PM2.5 mass, effect estimates of K, Ni, S, and V were slightly attenuated, whereas effect estimates of Cu, Si, Fe, and Zn became null or negative. ConclusionsOur results point towards an increased risk of lung cancer in connection with sources of combustion particles from oil and biomass burning and secondary inorganic aerosols rather than non-exhaust traffic emissions. Specific limit values or guidelines targeting these specific PM2.5 components may prove helpful in future lung cancer prevention strategies.

Residential Exposure to PM2.5 Components and Risk of Childhood Non-Hodgkin Lymphoma in Denmark: A Nationwide Register-Based Case-Control Study.

In a recent study, we observed an increased risk of childhood non-Hodgkin lymphoma (NHL) associated with exposure to fine atmospheric particulate matter (PM2.5) and black carbon (BC). In this nationwide register-based case-control study, we focus on specific components of PM2.5 in relation to childhood NHL in Denmark (1981–2013) by identifying all incidents of childhood NHL cases in the Danish Cancer Registry (n = 170) and four (cancer-free) randomly selected controls matched by date of birth and sex. We applied PM2.5 concentrations and the following sub-components: secondary organic aerosols (SOA), secondary inorganic aerosols (SIA; i.e., NO3−, NH4+ and SO42−), BC, organic carbon (OC) and sea salt. We calculated a time-weighted exposure average from birth to index-date at all addresses. Odds ratios (ORs) were adjusted for register-based socio-demographic variables. We observed adjusted ORs and 95% confidence intervals (95% CI) of 2.05 (1.10, 3.83) per interquartile range (IQR, 4.83 µg/m3) PM2.5 and 1.73 (0.68, 4.41) per IQR (3.71 µg/m3) SIA, 0.95 (0.71, 1.29) per IQR (0.05 µg/m3) SOA, 1.22 (1.02, 1.46) per IQR (0.39 µg/m3) BC, 1.02 (0.83, 1.26) per IQR (0.56 µg/m3) OC and 1.01 (0.79, 1.30) per IQR (0.87 µg/m3) sea salt, respectively. The estimates were attenuated after adjustment for PM2.5, whereas the OR for PM2.5 remained increased regardless of adjustment for specific components. The findings indicate that the previously observed relation between PM2.5 and childhood NHL may be related to BC (as reported in our previous study) but also partly to SIA, but the role of specific chemical components of PM2.5 remains ambiguous.