Is ambient air pollution associated with sarcopenia? Results from a nation-wide cross-sectional study.

BACKGROUND: sarcopenia is a disease that involves the degeneration of muscle strength, muscle mass and physical performance. It remains unknown whether air pollution exposure increases the risk of sarcopenia. METHODS: the baseline survey of the UK Biobank was used in this study. Sarcopenia was identified according to European Working Group on Sarcopenia in Older People 2 (EWGSOP2) and classified into non-sarcopenia and probable sarcopenia. Land use regressions were used to estimate concentrations of particulate matter (PM2.5), coarse particles (PMcoarse), PM10, PM2.5 absorbance, nitrogen dioxide (NO2) and nitrogen oxides (NOx). Logistic regression models were applied to estimate the associations between air pollution and sarcopenia and its components. RESULTS: out of 352,265 participants, 28,710 (8.2%) were identified with probable sarcopenia. In adjusted models, there were increased odds of probable sarcopenia for each interquartile range increase in PM2.5 (OR: 1.06; 95% CI: 1.04, 1.07), PM10 (OR: 1.15; 95% CI: 1.13, 1.17), PMcoarse (OR: 1.02; 95% CI:1.01, 1.03), PM2.5 absorbance (OR: 1.08; 95% CI: 1.07, 1.10), NO2 (OR: 1.12; 95% CI:1.10, 1.14) and NOx (OR: 1.06; 95% CI: 1.05, 1.08). CONCLUSIONS: this study suggests that exposure to ambient air pollution might be one risk factor of sarcopenia. Prospective studies are needed to further confirm our findings.

Ambient air pollution and ovarian cancer survival in California.

OBJECTIVE: To examine whether exposure to ambient ozone, particulate matter with diameter less than 2.5 µm (PM2.5), nitrogen dioxide (NO2), and distance to major roadways (DTR) impact ovarian cancer-specific survival, while considering differences by stage, race/ethnicity, and socioeconomic status. METHODS: Women diagnosed with epithelial ovarian cancer from 1996 to 2014 were identified through the California Cancer Registry and followed through 2016. Women's geocoded addresses were linked to pollutant exposure data and averaged over the follow-up period. Pollutants were considered independently and in multi-pollutant models. Cox proportional hazards models assessed hazards of disease-specific death due to environmental exposures, controlling for important covariates, with additional models stratified by stage at diagnosis, race/ethnicity and socioeconomic status. RESULTS: PM2.5 and NO2, but not ozone or DTR, were significantly associated with survival in univariate models. In a multi-pollutant model for PM2.5, ozone, and DTR, an interquartile range increase in PM2.5 (Hazard Ratio [HR], 1.45; 95% Confidence Interval [CI], 1.41-1.49) was associated with worse prognosis. Similarly, in the multi-pollutant model with NO2, ozone, and DTR, women with higher NO2 exposures (HR for 20.0-30.0 ppb, 1.30; 95% CI, 1.25-1.36 and HR for >30.0 ppb, 2.48; 95% CI, 2.32-2.66) had greater mortality compared to the lowest exposed (<20.0 ppb). Stratified results show the effects of the pollutants differed by race/ethnicity and were magnified among women diagnosed in early stages. CONCLUSIONS: Our analyses suggest that greater exposure to NO2 and PM2.5 may adversely impact ovarian cancer-specific survival, independent of sociodemographic and treatment factors. These findings warrant further study.

Role of nitroxyl (HNO) in cardiovascular system: From biochemistry to pharmacology.

Cardiovascular diseases are recognized to be a major cause of people morbidity and mortality. A host of stress signals contribute to the pathogenesis of cardiovascular disorders. Deficiency of hydrogen sulfide (H2S) or nitric oxide (NO) coordinately plays essential roles in the development of cardiovascular diseases. Recent studies have shown that interaction between the two gaseostransmitters, H2S and NO, may give rise to nitroxyl (HNO), one-electron-reduced product of NO. HNO is found to exhibit a variety of biological and pharmacological properties including positive inotropy and cardiovascular protective effects, etc. In this review, recent progresses regarding HNO generation, detection, biochemical and pharmacological functions are discussed.

Immune biomarkers link air pollution exposure to blood pressure in adolescents.

BACKGROUND: Childhood exposure to air pollution contributes to cardiovascular disease in adulthood. Immune and oxidative stress disturbances might mediate the effects of air pollution on the cardiovascular system, but the underlying mechanisms are poorly understood in adolescents. Therefore, we aimed to identify immune biomarkers linking air pollution exposure and blood pressure levels in adolescents. METHODS: We randomly recruited 100 adolescents (mean age, 16 years) from Fresno, California. Using central-site data, spatial-temporal modeling, and distance weighting exposures to the participant's home, we estimated average pollutant levels [particulate matter (PM), polyaromatic hydrocarbons (PAH), ozone (O3), carbon monoxide (CO) and nitrogen oxides (NOx)]. We collected blood samples and vital signs on health visits. Using proteomic platforms, we quantitated markers of inflammation, oxidative stress, coagulation, and endothelial function. Immune cellular characterization was performed via mass cytometry (CyTOF). We investigated associations between pollutant levels, cytokines, immune cell types, and blood pressure (BP) using partial least squares (PLS) and linear regression, while adjusting for important confounders. RESULTS: Using PLS, biomarkers explaining most of the variance in air pollution exposure included markers of oxidative stress (GDF-15 and myeloperoxidase), acute inflammation (C-reactive protein), hemostasis (ADAMTS, D-dimer) and immune cell types such as monocytes. Most of these biomarkers were independently associated with the air pollution levels in fully adjusted regression models. In CyTOF analyses, monocytes were enriched in participants with the highest versus the lowest PM2.5 exposure. In both PLS and linear regression, diastolic BP was independently associated with PM2.5, NO, NO2, CO and PAH456 pollution levels (P ≤ 0.009). Moreover, monocyte levels were independently related to both air pollution and diastolic BP levels (P ≤ 0.010). In in vitro cell assays, plasma of participants with high PM2.5 exposure induced endothelial dysfunction as evaluated by eNOS and ICAM-1 expression and tube formation. CONCLUSIONS: For the first time in adolescents, we found that ambient air pollution levels were associated with oxidative stress, acute inflammation, altered hemostasis, endothelial dysfunction, monocyte enrichment and diastolic blood pressure. Our findings provide new insights on pollution-related immunological and cardiovascular disturbances and advocate preventative measures of air pollution exposure.

Increased Chronic Obstructive Pulmonary Disease Exacerbations of Likely Viral Etiology Follow Elevated Ambient Nitrogen Oxides.

RATIONALE: Epidemiologic research strongly supports an association between air pollution and chronic obstructive pulmonary disease exacerbations. Numerous mechanisms may underlie any association because pollutants are toxic to pulmonary cells and may increase susceptibility to respiratory infections. The relationship between ambient pollution and exacerbation etiology has not been studied. OBJECTIVES: To evaluate the characteristics of pollution-associated exacerbations and whether the association is specific to exacerbations of infective or noninfective etiology. METHODS: We analyzed the effect of preceding ambient particulate matter less than or equal to 10 µm in aerodynamic diameter, oxides of nitrogen (NOx), and ozone on characterized chronic obstructive pulmonary disease exacerbations in a regression model adjusted for temperature, seasonality, and long-term trend. We specifically examined associations with exacerbations of suspected viral and/or bacterial, or noninfective etiology. For the associations identified we further examined the characteristics of pollution-associated exacerbations. MEASUREMENTS AND MAIN RESULTS: A total of 4,173 exacerbations occurred over the 20-year study period. Higher ambient NOx was consistently associated with increased viral-type exacerbations at 2-4 days lag (P = 0.010). Recovery for viral-type exacerbations after higher ambient NOx was significantly prolonged. These findings were consistent in the subset of 2,841 exacerbations treated with oral corticosteroids or antibiotics, with recovery 1.29 (95% confidence interval, 1.17-1.42; P < 0.001) times longer with viral-type exacerbations of onset 3 days after above- versus below-median ambient NOx. A likely bimodal association of particulate matter less than or equal to 10 µm in aerodynamic diameter with infective exacerbations was also evident and supported by a daily time-series analysis. CONCLUSIONS: Higher levels of ambient NOx are associated with prolonged exacerbations of likely viral etiology, supporting toxicologic effects of air pollution that increase susceptibility to, and severity of, infection.

Treatments targeting inotropy.

Acute heart failure (HF) and in particular, cardiogenic shock are associated with high morbidity and mortality. A therapeutic dilemma is that the use of positive inotropic agents, such as catecholamines or phosphodiesterase-inhibitors, is associated with increased mortality. Newer drugs, such as levosimendan or omecamtiv mecarbil, target sarcomeres to improve systolic function putatively without elevating intracellular Ca2+. Although meta-analyses of smaller trials suggested that levosimendan is associated with a better outcome than dobutamine, larger comparative trials failed to confirm this observation. For omecamtiv mecarbil, Phase II clinical trials suggest a favourable haemodynamic profile in patients with acute and chronic HF, and a Phase III morbidity/mortality trial in patients with chronic HF has recently begun. Here, we review the pathophysiological basis of systolic dysfunction in patients with HF and the mechanisms through which different inotropic agents improve cardiac function. Since adenosine triphosphate and reactive oxygen species production in mitochondria are intimately linked to the processes of excitation-contraction coupling, we also discuss the impact of inotropic agents on mitochondrial bioenergetics and redox regulation. Therefore, this position paper should help identify novel targets for treatments that could not only safely improve systolic and diastolic function acutely, but potentially also myocardial structure and function over a longer-term.

Long-Term Exposure to Air Pollution and Survival After Ischemic Stroke.

Background and Purpose- China bears a heavy burden of stroke because of its large population of elderly people and the propensity for stroke. Previous studies have examined the association between air pollution and stroke mortality or hospital admission. However, the global evidence for adverse effects of air pollution on survival after stroke is scarce. Methods- We used the first national hospital-based prospective registry cohort of stroke in China, which included 12 291 ischemic stroke patients who visited hospitals during 2007 to 2008. All patients were followed for 1-year poststroke. Deaths during the follow-up period were recorded. Participants' 3-year prestroke exposures to ambient PM1, PM2.5, PM10 (particulate matter with aerodynamic diameters ≤1, ≤2.5, and ≤10 µm, respectively) and NO2 (nitrogen dioxide) were estimated by machine learning algorithms with satellite remote sensing, land use information, and meteorological data. Cox proportional hazards models were used to examine the association between air pollution and survival after ischemic stroke. Results- In total, 1649 deaths were identified during the 1-year follow-up period. After controlling for potential confounders, significant associations were observed between exposure to PM1 and PM2.5 and incident fatal ischemic stroke. The corresponding hazard ratios and 95% CIs associated with 10 µg/m3 increase in PM1 and PM2.5 were 1.05 (1.02-1.09) and 1.03 (1.00-1.06), respectively. No significant association was observed for PM10 or NO2 (hazard ratios and 95% CIs, 1.01 [1.00-1.03] and 1.03 [0.99-1.06], respectively). Higher hazard ratios (and 95% CIs) were observed for male, elderly and obese individuals. Conclusions- Prestroke exposure to PM1 and PM2.5 was associated with increased incident fatal ischemic stroke in the year following an ischemic stroke in China. Improved air quality may be beneficial for people to recover from stroke.

Ambient air pollution and pulmonary vascular volume on computed tomography: the MESA Air Pollution and Lung cohort studies.

BACKGROUND: Air pollution alters small pulmonary vessels in animal models. We hypothesised that long-term ambient air pollution exposure would be associated with differences in pulmonary vascular volumes in a population-based study. METHODS: The Multi-Ethnic Study of Atherosclerosis recruited adults in six US cities. Personalised long-term exposures to ambient black carbon, nitrogen dioxide (NO2), oxides of nitrogen (NO x ), particulate matter with a 50% cut-off aerodynamic diameter of <2.5 µm (PM2.5) and ozone were estimated using spatiotemporal models. In 2010-2012, total pulmonary vascular volume was measured as the volume of detectable pulmonary arteries and veins, including vessel walls and luminal blood volume, on noncontrast chest computed tomography (TPVVCT). Peripheral TPVVCT was limited to the peripheral 2 cm to isolate smaller vessels. Linear regression adjusted for demographics, anthropometrics, smoking, second-hand smoke, renal function and scanner manufacturer. RESULTS: The mean±sd age of the 3023 participants was 69.3±9.3 years; 46% were never-smokers. Mean exposures were 0.80 µg·m-3 black carbon, 14.6 ppb NO2 and 11.0 µg·m-3 ambient PM2.5. Mean±sd peripheral TPVVCT was 79.2±18.2 cm3 and TPVVCT was 129.3±35.1 cm3. Greater black carbon exposure was associated with a larger peripheral TPVVCT, including after adjustment for city (mean difference 0.41 (95% CI 0.03-0.79) cm3 per interquartile range; p=0.036). Associations for peripheral TPVVCT with NO2 were similar but nonsignificant after city adjustment, while those for PM2.5 were of similar magnitude but nonsignificant after full adjustment. There were no associations for NO x or ozone, or between any pollutant and TPVVCT. CONCLUSIONS: Long-term black carbon exposure was associated with a larger peripheral TPVVCT, suggesting diesel exhaust may contribute to remodelling of small pulmonary vessels in the general population.

Long-term exposure to air pollution and hospitalization for dementia in the Rome longitudinal study.

BACKGROUND: Few studies have explored the role of air pollution in neurodegenerative processes, especially various types of dementia. Our aim was to evaluate the association between long-term exposure to air pollution and first hospitalization for dementia subtypes in a large administrative cohort. METHODS: We selected 350,844 subjects (free of dementia) aged 65-100 years at inclusion (21/10/2001) and followed them until 31/12/2013. We selected all subjects hospitalized for the first time with primary or secondary diagnoses of various forms of dementia. We estimated the exposure at residence using land use regression models for nitrogen oxides (NOx, NO2) and particulate matter (PM) and a chemical transport model for ozone (O3). We used Cox models to estimate the association between exposure and first hospitalization for dementia and its subtypes: vascular dementia (Vd), Alzheimer's disease (Ad) and senile dementia (Sd). RESULTS: We selected 21,548 first hospitalizations for dementia (7497 for Vd, 7669 for Ad and 7833 for Sd). Overall, we observed a negative association between exposure to NO2 (10 µg/m3) and dementia hospitalizations (HR = 0.97; 95% CI: 0.96-0.99) and a positive association between exposure to O3, NOx and dementia hospitalizations, (O3: HR = 1.06; 95% CI: 1.04-1.09 per 10 µg/m3; NOx: HR = 1.01; 95% CI: 1.00-1.02 per 20 µg/m3).H. Exposure to NOx, NO2, PM2.5, and PM10 was positively associated with Vd and negatively associated with Ad. Hospitalization for Sd was positively associated with exposure to O3 (HR = 1.20; 95% CI: 1.15-1.24 per 10 µg/m3). CONCLUSIONS: Our results showed a positive association between exposure to NOx and O3 and hospitalization for dementia and a negative association between NO2 exposure and hospitalization for dementia. In the analysis by subtype, exposure to each pollutants (except O3) demonstrated a positive association with vascular dementia, while O3 exposure was associated with senile dementia. The results regarding vascular dementia are a clear indication that the brain effects of air pollution are linked with vascular damage.

Association Between Long-term Exposure to Ambient Air Pollution and Change in Quantitatively Assessed Emphysema and Lung Function.

Importance: While air pollutants at historical levels have been associated with cardiovascular and respiratory diseases, it is not known whether exposure to contemporary air pollutant concentrations is associated with progression of emphysema. Objective: To assess the longitudinal association of ambient ozone (O3), fine particulate matter (PM2.5), oxides of nitrogen (NOx), and black carbon exposure with change in percent emphysema assessed via computed tomographic (CT) imaging and lung function. Design, Setting, and Participants: This cohort study included participants from the Multi-Ethnic Study of Atherosclerosis (MESA) Air and Lung Studies conducted in 6 metropolitan regions of the United States, which included 6814 adults aged 45 to 84 years recruited between July 2000 and August 2002, and an additional 257 participants recruited from February 2005 to May 2007, with follow-up through November 2018. Exposures: Residence-specific air pollutant concentrations (O3, PM2.5, NOx, and black carbon) were estimated by validated spatiotemporal models incorporating cohort-specific monitoring, determined from 1999 through the end of follow-up. Main Outcomes and Measures: Percent emphysema, defined as the percent of lung pixels less than -950 Hounsfield units, was assessed up to 5 times per participant via cardiac CT scan (2000-2007) and equivalent regions on lung CT scans (2010-2018). Spirometry was performed up to 3 times per participant (2004-2018). Results: Among 7071 study participants (mean [range] age at recruitment, 60 [45-84] years; 3330 [47.1%] were men), 5780 were assigned outdoor residential air pollution concentrations in the year of their baseline examination and during the follow-up period and had at least 1 follow-up CT scan, and 2772 had at least 1 follow-up spirometric assessment, over a median of 10 years. Median percent emphysema was 3% at baseline and increased a mean of 0.58 percentage points per 10 years. Mean ambient concentrations of PM2.5 and NOx, but not O3, decreased substantially during follow-up. Ambient concentrations of O3, PM2.5, NOx, and black carbon at study baseline were significantly associated with greater increases in percent emphysema per 10 years (O3: 0.13 per 3 parts per billion [95% CI, 0.03-0.24]; PM2.5: 0.11 per 2 µg/m3 [95% CI, 0.03-0.19]; NOx: 0.06 per 10 parts per billion [95% CI, 0.01-0.12]; black carbon: 0.10 per 0.2 µg/m3 [95% CI, 0.01-0.18]). Ambient O3 and NOx concentrations, but not PM2.5 concentrations, during follow-up were also significantly associated with greater increases in percent emphysema. Ambient O3 concentrations, but not other pollutants, at baseline and during follow-up were significantly associated with a greater decline in forced expiratory volume in 1 second per 10 years (baseline: 13.41 mL per 3 parts per billion [95% CI, 0.7-26.1]; follow-up: 18.15 mL per 3 parts per billion [95% CI, 1.59-34.71]). Conclusions and Relevance: In this cohort study conducted between 2000 and 2018 in 6 US metropolitan regions, long-term exposure to ambient air pollutants was significantly associated with increasing emphysema assessed quantitatively using CT imaging and lung function.

Genetic variation in biotransformation enzymes, air pollution exposures, and risk of spina bifida.

Spina bifida is a birth defect characterized by incomplete closure of the embryonic neural tube. Genetic factors as well as environmental factors have been observed to influence risks for spina bifida. Few studies have investigated possible gene-environment interactions that could contribute to spina bifida risk. The aim of this study is to examine the interaction between gene variants in biotransformation enzyme pathways and ambient air pollution exposures and risk of spina bifida. We evaluated the role of air pollution exposure during pregnancy and gene variants of biotransformation enzymes from bloodspots and buccal cells in a California population-based case-control (86 cases of spina bifida and 208 non-malformed controls) study. We considered race/ethnicity and folic acid vitamin use as potential effect modifiers and adjusted for those factors and smoking. We observed gene-environment interactions between each of the five pollutants and several gene variants: NO (ABCC2), NO2 (ABCC2, SLC01B1), PM10 (ABCC2, CYP1A1, CYP2B6, CYP2C19, CYP2D6, NAT2, SLC01B1, SLC01B3), PM2.5 (CYP1A1 and CYP1A2). These analyses show positive interactions between air pollution exposure during early pregnancy and gene variants associated with metabolizing enzymes. These exploratory results suggest that some individuals based on their genetic background may be more susceptible to the adverse effects of pollution.

Air pollution and airway resistance at age 8 years - the PIAMA birth cohort study.

BACKGROUND: Air pollution has been found to adversely affect children's lung function. Forced expiratory volume in 1 s and forced vital capacity from spirometry have been studied most frequently, but measurements of airway resistance may provide additional information. We assessed associations of long-term air pollution exposure with airway resistance. METHODS: We measured airway resistance at age 8 with the interrupter resistance technique (Rint) in participants of the Dutch PIAMA birth cohort study. We linked Rint with estimated annual average air pollution concentrations [nitrogen oxides (NO2, NOx), PM2.5 absorbance ("soot"), and particulate matter < 2.5 µm (PM2.5), < 10 µm (PM10) and 2.5-10 µm (PMcoarse)] at the birth address and current home address (n = 983). Associations between air pollution exposure and interrupter resistance (Rint) were assessed using multiple linear regression adjusting for potential confounders. RESULTS: We found that higher levels of NO2 at the current address were associated with higher Rint [adj. mean difference (95% confidence interval) per interquartile range increase in NO2: 0.018 (0.001, 0.035) kPa·s·L- 1]. Similar trends were observed for the other pollutants, except, PM10. No association was found between Rint and exposure at the birth address. CONCLUSIONS: Our results support the hypothesis that air pollution exposure is associated with a lower lung function in schoolchildren.

The effect of industry-related air pollution on lung function and respiratory symptoms in school children.

BACKGROUND: Heavy industry emits many potentially hazardous pollutants into the air which can affect health. However, the effects of air pollution from heavy industry on lung function and respiratory symptoms have been investigated scarcely. Our aim was to investigate the associations of long-term air pollution from heavy industry with lung function and respiratory symptoms in school children. METHODS: A cross-sectional lung function study was conducted among school children (7-13 years) in the vicinity of an area with heavy industry. Lung function measurements were conducted during school hours. Parents of the children were asked to complete a questionnaire about the health of their children. A dispersion model was used to characterize the additional individual-level exposures to air pollutants from the industry in the area. Associations between PM2.5 and NOX exposure with lung function and presence of respiratory symptoms were investigated by linear and/or logistic regression analysis. RESULTS: Participation in the lung function measurements and questionnaires was 84% (665/787) and 77% (603/787), respectively. The range of the elevated PM2.5 and NOX five years average concentrations (2008-2012) due to heavy industry were 0.04-1.59 µg/m3 and 0.74-11.33 µg/m3 respectively. After adjustment for confounders higher exposure to PM2.5 and NOX (per interquartile range of 0.56 and 7.43 µg/m3 respectively) was associated with lower percent predicted peak expiratory flow (PEF) (B -2.80%, 95%CI -5.05% to - 0.55% and B -3.67%, 95%CI -6.93% to - 0.42% respectively). Higher exposure to NOX (per interquartile range of 7.43 µg/m3) was also associated with lower percent forced vital capacity (FVC) and percent predicted forced expiration volume in 1 s (FEV1) (B -2.30, 95% CI -4.55 to - 0.05 and B -2.73, 95%CI -5.21 to - 0.25 respectively). No significant associations were found between the additional exposure to PM2.5 or NOX and respiratory symptoms except for PM2.5 and dry cough (OR 1.40, 95%CI 1.00 to 1.94). CONCLUSION: Exposure to PM2.5 and NOX from industry was associated with decreased lung function. Exposure to PM2.5 was also associated with parents' reports of dry cough among their children.

Influence of Gaseous Pollutants on COPD Exacerbations in Patients with Cardiovascular Comorbidities.

Exacerbations of chronic obstructive pulmonary disease (COPD) are a serious public health issue. Ambient pollution and meteorological factors are considered among precipitating factors. There are few data concerning the impact of ambient pollutants other than particulates on COPD exacerbations. Among gaseous pollutants four main groups of substances are primarily monitored: nitrogen oxides (NOx), sulphur dioxide (SO2), carbon monoxide (CO), and ozone (O3). In this study, 12,889 hospitalizations in the years 2006-2014 due to exacerbations of COPD in patients having a co-existing cardiovascular pathology were retrospectively analyzed. Cardiovascular disease was ruled out as the underlying reason of hospitalization. Data concerning the then accompanying gaseous pollutants and weather conditions were collected. The findings were that the impact of SO2 content was significantly associated with the relative risk (RR) of COPD exacerbation when the exposure took place at least 30 days or longer before hospital admission (RR 1.04-1.05; p < 0.05). In contrast, risk of COPD exacerbation rose when a shortening of the time lag between exposure to NOx and hospital admission was considered (RR 1.02-1.04; p < 0.05). O3 exposure was associated with a lower risk irrespective of the length of exposure/exacerbation lag (RR 0.77-0.90; p < 0.05). There were insignificant associations observed for CO. In conclusion, the study demonstrates a salient influence of a co-existing cardiovascular malady on the appearance of COPD-related respiratory exacerbations when the pollutant SO2 and NOx contents rose. In contrast, higher O3 content was associated with a lower risk of COPD exacerbation.

NOXious gases and the unpredictability of emerging plant pathogens under climate change.

Emerging pathogens of crops threaten food security and are increasingly problematic due to intensive agriculture and high volumes of trade and transport in plants and plant products. The ability to predict pathogen risk to agricultural regions would therefore be valuable. However, predictions are complicated by multi-faceted relationships between crops, their pathogens, and climate change. Climate change is related to industrialization, which has brought not only a rise in greenhouse gas emissions but also an increase in other atmospheric pollutants. Here, we consider the implications of rising levels of reactive nitrogen gases and their manifold interactions with crops and crop diseases.

Ambient Air Pollution and Risk of Gestational Hypertension.

Air pollution has been linked to hypertension in the general population, but data on gestational hypertension (GH) are limited. We investigated criteria air pollutants and air toxics during the period before conception and in early gestation in relation to GH risk in the Consortium on Safe Labor/Air Quality and Reproductive Health Study (United States, 2002-2008). Modified Community Multi-scale Air Quality models estimated air pollution exposures for 6,074 singleton pregnancies in which GH was present and 199,980 normotensive pregnancies. Generalized estimating equations estimated relative risks per interquartile-range increment for pollutants and high exposure (≥75th percentile) for air toxics after adjustment for major risk factors. For an interquartile-range increment, GH risk was significantly increased by 18% for sulfur dioxide during the 3 months before conception and, during gestational weeks 1-20, 17% for nitrogen oxides, 10% for particulate matter with an aerodynamic diameter <2.5 µm, 7% for particulate matter with an aerodynamic diameter <10 µm, and 22% for sulfur dioxide. High exposures to several polycyclic aromatic hydrocarbons before conception and during the first trimester were significantly associated with 8%-20% higher risk of GH. Further, preconceptional exposures to several volatile organic compounds were significantly associated with 11%-19% higher risk. Our findings suggest that early exposures to criteria air pollutants, particularly from transport emissions, and high exposure to several air toxics before conception may increase GH risk.

Ambient air pollution and primary liver cancer incidence in four European cohorts within the ESCAPE project.

BACKGROUND: Tobacco smoke exposure increases the risk of cancer in the liver, but little is known about the possible risk associated with exposure to ambient air pollution. OBJECTIVES: We evaluated the association between residential exposure to air pollution and primary liver cancer incidence. METHODS: We obtained data from four cohorts with enrolment during 1985-2005 in Denmark, Austria and Italy. Exposure to nitrogen oxides (NO2 and NOX), particulate matter (PM) with diameter of less than 10µm (PM10), less than 2.5µm (PM2.5), between 2.5 and 10µm (PM2.5-10) and PM2.5 absorbance (soot) at baseline home addresses were estimated using land-use regression models from the ESCAPE project. We also investigated traffic density on the nearest road. We used Cox proportional-hazards models with adjustment for potential confounders for cohort-specific analyses and random-effects meta-analyses to estimate summary hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS: Out of 174,770 included participants, 279 liver cancer cases were diagnosed during a mean follow-up of 17 years. In each cohort, HRs above one were observed for all exposures with exception of PM2.5 absorbance and traffic density. In the meta-analysis, all exposures were associated with elevated HRs, but none of the associations reached statistical significance. The summary HR associated with a 10-µg/m3 increase in NO2 was 1.10 (95% confidence interval (CI): 0.93, 1.30) and 1.34 (95% CI: 0.76, 2.35) for a 5-µg/m3 increase in PM2.5. CONCLUSIONS: The results provide suggestive evidence that ambient air pollution may increase the risk of liver cancer. Confidence intervals for associations with NO2 and NOX were narrower than for the other exposures.

Emission Standards, Public Transit, and Infant Health.

Transit buses are an integral part of urban life. They reduce externalities generated from private vehicles and increase geographic mobility. However, unlike most private vehicles in the United States, they use diesel fuel and emit higher amounts of toxic pollutants. The U.S. Environmental Protection Agency set emission standards for transit buses starting in 1988 that have been continually updated, but their public health and economic impacts are unclear due to scarce emissions data. I construct a novel panel dataset for the New York City (NYC) Transit bus fleet between 1990 and 2009 and examine the impact of bus pollution on infant health by using bus vintage as a proxy for emissions. I exploit the variation in vintage as older buses are retired and replaced with newer, lower-emitting buses forced to adhere to stricter emission standards. I then assign maternal exposure to bus vintage at the census block level. Findings suggest that maternal exposure to the oldest, unregulated buses is associated with modest reductions in birth weight and gestational age relative to newer buses that abide by emissions policies. I then conduct a back-of-the-envelope cost-benefit calculation and find net economic benefits of $53.3 million resulting from improved emission standards for the 2009 birth cohort in NYC. Since the treatment in this study clearly maps to federal emissions policies, these results are the first to provide credible evidence that transit bus emission standards had a positive effect on infant health.

Ambient air pollution and risk of tuberculosis: a cohort study.

OBJECTIVES: Several respirable hazards, including smoking and indoor air pollution from biomass, were suggested to increase the risk of tuberculosis. Few studies have been conducted on ambient air pollution and tuberculosis. We investigated the association between exposure to ambient air pollution and incidence of active tuberculosis. METHODS: We conducted a cohort study using 106,678 participants of a community-based screening service in Taiwan, 2005-2012. We estimated individual exposure to air pollution using data from the nearest air quality monitoring station and the road intensity within a 500 m buffer zone. The incidence of tuberculosis was ascertained from the national tuberculosis registry. RESULTS: After a median follow-up of 6.7 years, 418 cases of tuberculosis occurred. Exposure to fine particulate matter (PM2.5) was associated with increased risk of active tuberculosis (adjusted HR: 1.39/10 µg/m3 (95% CI 0.95 to 2.03)). In addition, traffic-related air pollution including nitrogen dioxide (adjusted HR: 1.33/10 ppb; 95% CI 1.04 to 1.70), nitrogen oxides (adjusted HR: 1.21/10 ppb; 95% CI 1.04 to 1.41) and carbon monoxide (adjusted HR: 1.89/ppm; 95% CI 0.78 to 4.58) was associated with tuberculosis risk. There was a non-significant trend between the length of major roads in the neighbourhood and culture-confirmed tuberculosis (adjusted HR: 1.04/km; 95% CI 0.995 to 1.09). CONCLUSIONS: Our study revealed a possible link between ambient air pollution and risk of active tuberculosis. Since people from developing countries continue to be exposed to high levels of ambient air pollution and to experience high rates of tuberculosis, the impact of worsening air pollution on global tuberculosis control warrants further investigation.