Air pollution disproportionately impairs beneficial invertebrates: a meta-analysis.

Air pollution has the potential to disrupt ecologically- and economically-beneficial services provided by invertebrates, including pollination and natural pest regulation. To effectively predict and mitigate this disruption requires an understanding of how the impacts of air pollution vary between invertebrate groups. Here we conduct a global meta-analysis of 120 publications comparing the performance of different invertebrate functional groups in unpolluted and polluted atmospheres. We focus on the pollutants ozone, nitrogen oxides, sulfur dioxide and particulate matter. We show that beneficial invertebrate performance is reduced by air pollution, whereas the performance of plant pest invertebrates is not significantly affected. Ozone pollution has the most detrimental impacts, and these occur at concentrations below national and international air quality standards. Changes in invertebrate performance are not dependent on air pollutant concentrations, indicating that even low levels of pollution are damaging. Predicted increases in tropospheric ozone could result in unintended consequences to global invertebrate populations and their valuable ecological services.

Effect of nitrogen oxides and sulfur oxides to triphenyl phosphate degradation and cytotoxicity on surface of different transition metal salts.

Nitrogen oxides and sulfur oxides, as the dominant toxic gases in the atmosphere, can induce severe human health problems under the composite pollutant conditions. Currently the effect of nitrogen or sulfur oxides in atmospheric environment to the degradation and cytotoxicity of triphenyl phosphate (TPhP) on atmospheric particle surfaces still remain poorly understood. Hence, laboratory simulation methods were used in this study to investigate the effect and related mechanism. First, particle samples were prepared with the TPhP coated on MnSO4, CuSO4, FeSO4 and Fe2(SO4)3 surface. The results showed that, when nitrogen or sulfur oxides were present, more significant TPhP degradation on all samples can be observed under both light and dark conditions. The results proved nitrogen oxides and sulfur oxides were the vital influence factors to the degradation of TPhP, which mainly promoted the OH generation in the polluted atmosphere. The mechanism study indicated that diphenyl hydrogen phosphate (DPhP) and OH-DPhP were two main stable degradation products. These degradation products originated from the phenoxy bond cleavage and hydroxylation of TPhP caused by hydroxyl radicals. In addition, no TPhP related organosulfates (OSs) or organic nitrates (ON) formation were observed. Regarding the cytotoxicity, all the particles can induce more significant cellular injury and apoptosis of A549 cells, which may be relevant to the adsorbed nitrogen oxides or sulfur oxides on particles surfaces. The superfluous reactive oxygen species (ROS) generation was the possible reason of cytotoxicity. This research can supply a comprehensive understanding of the promoting effect of nitrogen and sulfur oxides to TPhP degradation and the composite cytotoxicity of atmospheric particles.

Air pollution, genetic factors and the risk of depression.

Both genetics and ambient air pollutants contribute to depression, but the degree to which genetic susceptibility modifies the effect of air pollution on depression remains unknown. We aimed to investigate the effect of the modification of genetic susceptibility on depression. Notably, 490,780 participants who were free of depression at baseline in the UK Biobank study were recruited from 2006 to 2010. A land use regression (LUR) model was performed to estimate the concentrations of particulate matter with diameters ranging from ≤2.5-≤10 µm (PM2.5, PM2.5-10 and PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOx). The International Classification of Diseases 10th Revision (ICD-10) code was used to identify depression cases. Cox proportional hazard models adjusted for covariates were used to investigate the association between ambient air pollutants and depression. Moreover, the polygenic risk score (PRS) was calculated to evaluate cumulative genetic effects, and additive interaction models were established to explore whether genetic susceptibility modified the effects of air pollutants on depression. PM2.5, PM10, NO2 and NOx exposure were significantly positively associated with the risk of depression, and the hazard ratios and 95 % confidence intervals for a 10-µg/m3 increase in PM2.5, PM10, NO2 and NOx concentrations were 2.12 (1.82, 2.47), 1.12 (1.03, 1.23), 1.07 (1.05, 1.10) and 1.04 (1.03, 1.05), respectively. Air pollutants and genetic variants exerted significant additive effects on the risk of depression (relative excess risk due to the interaction [RERI]: 0.15 for PM2.5, 0.12 for PM10, 0.10 for NO2, and 0.12 for NOx; attributable proportion due to the interaction [AP]: 0.12 for PM2.5, 0.10 for PM10, 0.08 for NO2, and 0.09 for NOx). Air pollution exposure was significantly associated with the risk of depression, and participants with a higher genetic risk were more likely to develop depression when exposed to high levels of air pollution.

Air Pollution, Genetic Factors, and the Risk of Lung Cancer: A Prospective Study in the UK Biobank.

Rationale: Both genetic and environmental factors contribute to lung cancer, but the degree to which air pollution modifies the impact of genetic susceptibility on lung cancer remains unknown. Objectives: To investigate whether air pollution and genetic factors jointly contribute to incident lung cancer. Methods: We analyzed data from 455,974 participants (53% women) without previous cancer at baseline in the UK Biobank. The concentrations of particulate matter (PM) (PM ⩽2.5 µm in aerodynamic diameter [PM2.5], coarse PM between 2.5 µm and 10 µm in aerodynamic diameter [PMcoarse], and PM ⩽10 µm in aerodynamic diameter [PM10]), nitrogen dioxide (NO2), and nitrogen oxides (NOx) were estimated by using land-use regression models, and the association between air pollutants and incident lung cancer was investigated by using a Cox proportional hazard model. Furthermore, we constructed a polygenic risk score and evaluated whether air pollutants modified the effect of genetic susceptibility on the development of lung cancer. Measurements and Main Results: The results showed significant associations between the risk of lung cancer and PM2.5 (hazard ratio [HR], 1.63; 95% confidence interval [CI], 1.33-2.01; per 5 µg/m3), PM10 (HR, 1.53; 95% CI, 1.20-1.96; per 10 µg/m3), NO2 (HR, 1.10; 95% CI, 1.05-1.15; per 10 µg/m3), and NOx (HR, 1.13; 95% CI, 1.07-1.18; per 20 µg/m3). There were additive interactions between air pollutants and the genetic risk. Compared with participants with low genetic risk and low air pollution exposure, those with high air pollution exposure and high genetic risk had the highest risk of lung cancer (PM2.5: HR, 1.71; 95% CI, 1.45-2.02; PM10: HR, 1.77; 95% CI, 1.50-2.10; NO2: HR, 1.77; 95% CI, 1.42-2.22; NOx: HR, 1.67; 95% CI, 1.43-1.95). Conclusions: Long-term exposure to air pollution may increase the risk of lung cancer, especially in those with high genetic risk.

Prenatal exposure to VOCs and NOx and lung function in preschoolers.

BACKGROUND: Several studies have shown that exposure to air pollutants affects lung growth and development and can result in poor respiratory health in early life. METHODS: We included a subsample of 772 Mexican preschoolers whose mothers participated in a Prenatal Omega-3 fatty acid Supplements, GRowth, And Development birth cohort study with the aim to evaluate the impact of prenatal exposure to volatile organic compounds and nitrogen oxides on lung function measured by oscillation tests. The preschoolers were followed until 5 years of age. Anthropometric measurements and forced oscillation tests were performed at 36, 48, and 60 months of age. Information on sociodemographic and health characteristics was obtained during follow up. Prenatal exposure to volatile organic compounds and nitrogen oxides was evaluated using a land use regression models and the association between them was tested using a lineal regression and longitudinal linear mixed effect models adjusting for potential confounders. RESULTS: Overall, the mean (standard deviation) of the measurements of respiratory system resistance and respiratory system reactance at 6, 8, and 10 Hz during the follow-up period was 11.3 (2.4), 11.1 (2.4), 10.3 (2.2) and -5.2 (1.6), -4.8 (1.7), and -4.6 hPa s L-1 (1.6), respectively. We found a significantly positive association between respiratory resistance (ßRrs6 = 0.011; 95%CI: 0.001, 0.023) (P < .05) and prenatal exposure to nitrogen dioxide and a marginally negatively association between respiratory reactance (ßXrs6 = -11.40 95%CI: -25.26, 1.17 and ßXrs8 = -11.91 95%CI: -26.51, 1.43) (P = .07) and prenatal exposure to xylene. CONCLUSION: Prenatal exposure to air pollutants was significantly associated with the alteration of lung function measured by oscillation tests in these preschool children.

Effect modifiers of lung function and daily air pollutant variability in a panel of schoolchildren.

BACKGROUND: Acute pollutant-related lung function changes among children varies across pollutants and lag periods. We examined whether short-term air pollutant fluctuations were related to daily lung function among a panel of children and whether these effects are modified by airway hyperresponsiveness, location and asthma severity. METHODS: Students from randomly selected grade 4 classrooms at seven primary schools in Durban, participated, together with asthmatic children from grades 3-6 (n=423). The schools were from high pollutant exposed communities (south) and compared with schools from communities with lower levels of pollution (north), with similar socioeconomic profiles. Interviews, spirometry and methacholine challenge testing were conducted. Bihourly lung function measurements were performed over a 3-week period in four phases. During all schooldays, students blew into their personal digital monitors every 1.5-2 hours. Nitrogen dioxide (NO2), nitrogen oxide (NO), sulphur dioxide and particulate matter (<10 µm diameter) (PM10) were measured at each school. Generalised estimating equations assessed lag effects, using single-pollutant (single or distributed lags) models. RESULTS: FEV1 declines ranged from 13 to 18 mL per unit increase in IQR for NO and 14-23 mL for NO2. Among the 5-day average models, a 20 mL and 30 mL greater drop in FEV1 per IQR for NO2 and NO, respectively, among those with airway hyperresponsiveness compared with those without. Effects were seen among those with normal airways. CONCLUSIONS: This first panel study in sub-Saharan Africa, showed significant declines in lung function, in response to NO and NO2 with effects modified by airway hyperresponsiveness or persistent asthma.

Association between exposure to air pollution and hippocampal volume in adults in the UK Biobank.

BACKGROUND: The hippocampus is important for memory processing. Several neuropsychiatric diseases including Alzheimer's disease are associated with reduced hippocampal volume, and further the hippocampus appears vulnerable to environmental insult. Air pollution has been associated with cardiovascular disease, abnormal brain structure, and cognitive deficits. OBJECTIVE: Because of hippocampal vulnerability to environmental insults and based on the association between exposure to air pollution and cognitive function and brain structure, we evaluated the association between exposure to toxins in air pollution and left and right hippocampal volume using brain-imaging and air-pollution data from the UK Biobank, a large community-based dataset. METHODS: We used regression modelling to evaluate the association between exposure to nitrogen dioxide, nitrogen oxides, PM2.5, PM2.5-10, and PM10. and left and right hippocampal volume controlling for age, sex, body-mass index, overall health, alcohol use, smoking, educational attainment, socioeconomic status, inverse distance from the nearest major road, and a measure of total brain volume. RESULTS: In these models, PM2.5 concentration was associated with smaller left hippocampal volume. None of the other measures of air pollution was associated with either left or right hippocampal volume, although interaction models provided some evidence that sex might moderate the relationship between air pollution and hippocampal volume. In adjusted models, age, sex, educational attainment, income, overall health, current smoking, alcohol intake, and body-mass index were associated with hippocampal volume. CONCLUSIONS: PM2.5 at levels found in the United Kingdom was associated with smaller left hippocampal volume. Additional associations between several covariates and hippocampal volumes indicate that hippocampal volume might be associated with several potentially modifiable variables.

Exposure to Nitro-PAHs interfere with germination and early growth of Hordeum vulgare via oxidative stress.

Nitrated polycyclic aromatic hydrocarbons (Nitro-PAHs) as important organic pollutants are ubiquitous in the atmospheric environment, agricultural soils and aquatic environments to pose a severe polluting risk. However, little is known about the mechanism of Nitro-PAHs genotoxicity in plants. We analyzed seeds germination, seedlings growth, and toxicity mechanism following 1-Nitropyrene treatment in Hordeum vulgare. Our results reveal that 1-NP treatment could be an inhibited agent on seeds germination and growth of roots and shoots. Additionally, the reduction of mitotic index and the increasing frequency of micronucleus suggest that 1-NP may pose a potential risk of genotoxicity in the plant. We further clarify that O2- and H2O2 radicals contribute to 1-NP stimulation induced oxidative damage. Our study provides insights into the role of Nitro-PAHs exposure on growth processing toxicity and genotoxicity in plant and provided a useful reference for the surveillance and risk management of Nitro-PAHs in environments.

Contaminación atmosférica, riesgo cardiovascular e hipertensión arterial / Air pollution, cardiovascular risk and hypertension

La contaminación atmosférica es un factor preocupante y con impacto sobre la salud pública. Múltiples estudios relacionan la exposición a contaminantes atmosféricos con el aumento de eventos cardiovasculares, mortalidad cardiovascular y mortalidad por todas las causas. También se ha demostrado relación entre el aumento de contaminación y la elevación de la presión arterial, así como con una mayor prevalencia de hipertensión arterial. Los contaminantes que desempeñan un papel más relevante en esta asociación son las partículas aéreas en suspensión, el dióxido de nitrógeno y el dióxido de azufre. El objetivo de esta revisión es entender los mecanismos implicados en este aumento y conocer las publicaciones más recientes que relacionan contaminación atmosférica, riesgo cardiovascular e hipertensión arterial

Air pollution is a worrying factor and has an impact on public health. Multiple studies relate exposure to air pollutants with an increase in cardiovascular events, cardiovascular mortality and mortality for all causes. A relationship has also been demonstrated between increased pollution and high blood pressure, as well as a higher prevalence of hypertension. Pollutants that play a more relevant role in this association are particulate matters, nitrogen dioxide and sulphur dioxide. The objective of this review is to understand the mechanisms involved in this increase and to find the most recent publications that relate pollution, cardiovascular risk and hypertension

Hazardous gases (CO, NOx, CH4 and C3H8) released from CO2 fertilizer unit lead to oxidative damage and degrades photosynthesis in strawberry plants.

CO2 boilers/direct heating systems used in greenhouses often lead to incomplete combustion, which results in the formation of hazardous gases, such as carbon monoxide (CO), nitroxide (NOX) and other hydrocarbons. In this study, strawberry plants that were grown on rockwool cubes were transferred to airtight bottles and treated with CO, NOX, CH4 and C3H8 gases for 1-48 hours. Oxidative damage due to hazardous gases was observed, as indicated by H2O2 and [Formula: see text] determination. Photosynthetic pigments were reduced, and stomatal guard cells were damaged and remained closed compared to the control. The activity of other photosynthetic parameters was negatively related to hazardous gases. Reduction in the expression of multiprotein complexes was highly observed under hazardous gas treatments. This study highlighted that hazardous gases (CO, NOX, CH4 and C3H8) emitted due to incomplete combustion of CO2 fertilization units/or direct heating systems resulted in the formation of ROS in shoots and limited photosynthetic metabolism. We predicted that major steps must be incorporated to improve the efficiency of CO2 boiler/heating systems to decrease the emission of these hazardous gases and other hydrocarbons and to reduce the observed risks that are key to the reduction of crops.

Cross-sectional and longitudinal analyses of outdoor air pollution exposure and cognitive function in UK Biobank.

Observational studies have shown consistently increased likelihood of dementia or mild cognitive impairment diagnoses in people with higher air pollution exposure history, but evidence has been less consistent for associations with cognitive test performance. We estimated the association between baseline neighbourhood-level exposure to airborne pollutants (particulate matter and nitrogen oxides) and (1) cognitive test performance at baseline and (2) cognitive score change between baseline and 2.8-year follow-up, in 86,759 middle- to older-aged adults from the UK Biobank general population cohort. Unadjusted regression analyses indicated small but consistent negative associations between air pollutant exposure and baseline cognitive performance. Following adjustment for a range of key confounders, associations were inconsistent in direction and of very small magnitude. The largest of these indicated that 1 interquartile range higher air pollutant exposure was associated on average with 0.35% slower reaction time (95% CI: 0.13, 0.57), a 2.92% higher error rate on a visuospatial memory test (95% CI: 1.24, 4.62), and numeric memory scores that were 0.58 points lower (95% CI: -0.96, -0.19). Follow-up analyses of cognitive change scores did not show evidence of associations. The findings indicate that in this sample, which is five-fold larger than any previous cross-sectional study, the association between air pollution exposure and cognitive performance was weak. Ongoing follow-up of the UK Biobank cohort will allow investigation of longer-term associations into old age, including longitudinal tracking of cognitive performance and incident dementia outcomes.

The mediating role of risk perception in the association between industry-related air pollution and health.

BACKGROUND: Heavy industry emits many potentially hazardous pollutants into the air which can affect health. Awareness about the potential health impacts of air pollution from industry can influence people's risk perception. This in turn can affect (self-reported) symptoms. Our aims were to investigate the associations of air pollution from heavy industry with health symptoms and to evaluate whether these associations are mediated by people's risk perception about local industry. METHODS: A cross-sectional questionnaire study was conducted among children (2-18 years) and adults (19 years and above) living in the direct vicinity of an area with heavy industry. A dispersion model was used to characterize individual-level exposures to air pollution emitted from the industry in the area. Associations between PM2.5 and NOX with presence of chronic diseases (adults) and respiratory symptoms (adults and children) were investigated by logistic regression analysis. Risk perception was indirectly measured by worries about local industry (0-10 scale). Mediation analyses were performed to investigate the role of mediation by these worries. RESULTS: The response was 54% (2,627/4,877). In adults exposure to modelled PM2.5 from industry (per µg/m3) was related with reported high blood pressure (OR 1.56, 95% CI 1.13-2.15) and exposure to modelled NOX (per µg/m3) was inversely related with cardiovascular diseases (OR 0.91, 95% CI 0.84-0.98). In children higher PM2.5 and NOX concentrations (per µg/m3) were related with wheezing (OR 2.00, 95% CI 1.24-3.24 and OR 1.13, 95% CI 1.06-1.21 respectively) and dry cough (OR 2.33, 95% CI 1.55-3.52 and OR 1.16, 95% CI 1.10-1.22 respectively). Parental worry about local industry was an important mediator in exposure-health relations in children (indirect effect between 19-28%). CONCLUSION: Exposure from industry was associated with self-reported reported high blood pressure among adults and respiratory symptoms among their children. Risk perception was found to mediate these associations for children.

[Residential cohort study on mortality and hospitalization in Viggiano and Grumento Nova Municipalities in the framework of HIA in Val d'Agri (Basilicata Region, Southern Italy)]. / Studio di coorte residenziale su mortalità e ricoveri nei Comuni di Viggiano e Grumento Nova nell'ambito della VIS in Val d'Agri (Basilicata).

OBJECTIVES: to evaluate the associations among the emissions produced by "Centro olio Val d'Agri" (COVA), with mortality and hospitalization of residents in the Viggiano and Grumento Nova Municipalities, located in Val d'Agri (Basilicata Region, Southern Italy). DESIGN: residential cohort study. SETTINGS AND PARTICIPANTS: Lagrangians dispersion models to estimate the level of exposure at the address of residence to NOX concentrations as tracers of COVA emissions. Based on the tertile of NOX distribution, individual exposure was classified and a Cox model analysis was performed (hazard ratio, HR, trend with relative 95%CI). The association among exposure to NOX and the cohort mortality/hospitalization was evaluated considering age, socioeconomic status, and distance from the high traffic density road. The cohort included 6,795 residents (73,270 person-years) in the period 2000-2014. MAIN OUTCOME MEASURES: causes of mortality and hospitalization due to cardio-respiratory diseases, recognised as associated to air pollution, with medium-short latency induction period, consistent with the period of operation at the COVA. RESULTS: increasing trends were observed on three exposure classes for mortality due to circulatory system diseases (HR trend: 1.19; 95%CI 1.02-1.39), stronger considering women (HR trend: 1.19; 95%CI 1.02-1.39). From hospitalizations results, an increased risk emerges for respiratory diseases (HR trend: 1.12; 95%CI 1.01-1.25) and, for women, for diseases of the circulatory system (HR trend: 1.19; 95%CI 1.03-1.38), for ischemic diseases (HR trend: 1.33; 95%CI 1.02-1.74) and respiratory diseases (HR trend: 1.22; 95%CI 1.03-1.46). CONCLUSIONS: the excesses of mortality and hospitalization emerged in areas most exposed to pollutants of industrial origin are relevant for preventive actions. It is recommended to define and implement a surveillance system for the entire resident population based on indicators of environmental pollution and related health outcomes on the basis of the scientific literature and the results achieved by the present study.

Ozone exposure and pulmonary effects in panel and human clinical studies: Considerations for design and interpretation.

A wealth of literature exists regarding the pulmonary effects of ozone, a photochemical pollutant produced by the reaction of nitrogen oxide and volatile organic precursors in the presence of sunlight. This paper focuses on epidemiological panel studies and human clinical studies of ozone exposure, and discusses issues specific to this pollutant that may influence study design and interpretation as well as other, broader considerations relevant to ozone-health research. The issues are discussed using examples drawn from the wider literature. The recent panel and clinical literature is also reviewed. Health outcomes considered include lung function, symptoms, and pulmonary inflammation. Issues discussed include adversity, reversibility, adaptation, variability in ozone exposure metric used and health outcomes evaluated, co-pollutants in panel studies, influence of temperature in panel studies, and multiple comparisons. Improvements in and standardization of panel study approaches are recommended to facilitate comparisons between studies as well as meta-analyses. Additional clinical studies at or near the current National Ambient Air Quality Standard (NAAQS) of 70 ppb are recommended, as are clinical studies in sensitive subpopulations such as asthmatics. IMPLICATIONS: The pulmonary health impacts of ozone exposure have been well documented using both epidemiological and chamber study designs. However, there are a number of specific methodological and related issues that should be considered when interpreting the results of these studies and planning additional research, including the standardization of exposure and health metrics to facilitate comparisons among studies.

Prenatal Exposure to Nitrogen Oxides and its Association with Birth Weight in a Cohort of Mexican Newborns from Morelos, Mexico.

BACKGROUND: The Child-Mother binomial is potentially susceptible to the toxic effects of pollutants because some chemicals interfere with placental transfer of nutrients, thus affecting fetal development, and create an increased the risk of low birth weight, prematurity and intrauterine growth restriction. OBJECTIVE: To evaluate the impact of prenatal exposure to nitrogen oxides (NOx) on birth weight in a cohort of Mexican newborns. METHODOLOGY: We included 745 mother-child pair participants of the POSGRAD cohort study. Information on socio-demographic characteristics, obstetric history, health history and environmental exposure during pregnancy were readily available and the newborns' anthropometric measurements were obtained at delivery. Prenatal NOx exposure assessment was evaluated using a Land-Use Regression predictive models considering local monitoring from 60 sites on the State of Morelos. The association between prenatal exposure to NOx and birth weight was estimated using a multivariate linear regression models. RESULTS: The average birth weight was 3217 ± 439 g and the mean of NOx concentration was 21 ppb (Interquartile range, IQR = 6.95 ppb). After adjusting for maternal age and other confounders, a significant birthweight reduction was observed for each IQR of NOx increase (ß = -39.61 g, 95% CI: -77.00; -2.21; p = 0.04). CONCLUSIONS: Our results provides evidence that prenatal NOx exposure has a negative effect on birth weight, which may influence the growth and future development of the newborn.

Measuring the impact of global tropospheric ozone, carbon dioxide and sulfur dioxide concentrations on biodiversity loss.

The aim of this study is to examine the impact of air pollutants, including mono-nitrogen oxides (NOx), nitrous oxide (N2O), sulfur dioxide (SO2), carbon dioxide emissions (CO2), and greenhouse gas (GHG) emissions on ecological footprint, habitat area, food supply, and biodiversity in a panel of thirty-four developed and developing countries, over the period of 1995-2014. The results reveal that NOx and SO2 emissions both have a negative relationship with ecological footprints, while N2O emission and real GDP per capita have a direct relationship with ecological footprints. NOx has a positive relationship with forest area, per capita food supply and biological diversity while CO2 emission and GHG emission have a negative impact on food production. N2O has a positive impact on forest area and biodiversity, while SO2 emissions have a negative relationship with them. SO2 emission has a direct relationship with per capita food production, while GDP per capita significantly affected per capita food production and food supply variability across countries. The overall results reveal that SO2, CO2, and GHG emissions affected potential habitat area, while SO2 and GHG emissions affected the biodiversity index. Trade liberalization policies considerably affected the potential habitat area and biological diversity in a panel of countries.

Association between PM2.5 and PM2.5 Constituents and Preterm Delivery in California, 2000-2006.

BACKGROUND: Particulate matter (PM) has been documented to contribute to preterm delivery. However, few studies have investigated the relationships between individual constituents of fine PM (PM2.5 ) and preterm delivery, and factors that may modify their associations. METHODS: In this study, we examined the associations between several prenatal exposure metrics to PM2.5 and 23 constituents of PM2.5 and preterm delivery in California from 2000 to 2006. In a retrospective cohort study including 231 637 births, we conducted logistic regression analyses adjusting for maternal, infant, temporal, geographic, and neighbourhood characteristics. RESULTS: We observed increased risk for preterm delivery with full-gestational exposure for several PM2.5 constituents. Per interquartile range increase, ammonium (21.2%, 95% confidence interval (CI) 17.1, 25.4), nitrate (18.1%, 95% CI 14.9, 21.4) and bromine (16.7%, 95% CI 13.2, 20.3) had some of the largest increased risks. Alternatively, some PM2.5 constituents were inversely associated with preterm delivery, including chlorine (-8.2%, 95% CI -10.3, -6.0), sodium (-13.2%, 95% CI -15.2, -11.3), sodium ion (-11.9%, 95% CI -14.1, -9.6) and vanadium (-19.2%, 95% CI -25.3, -12.6). Greater associations between PM2.5 constituents and preterm delivery were observed for Blacks and Asians, older mothers, and those with some college education compared to their reference groups, as well as for births with gestational ages from 32 to 34 weeks. CONCLUSIONS: PM2.5 constituents ammonium, nitrate and bromine, often linked to traffic and biomass combustion, were most associated with increased risk of preterm delivery in California. Certain demographic subgroups may be particularly impacted.

Modeling variability in air pollution-related health damages from individual airport emissions.

In this study, we modeled concentrations of fine particulate matter (PM2.5) and ozone (O3) attributable to precursor emissions from individual airports in the United States, developing airport-specific health damage functions (deaths per 1000t of precursor emissions) and physically-interpretable regression models to explain variability in these functions. We applied the Community Multiscale Air Quality model using the Decoupled Direct Method to isolate PM2.5- or O3-related contributions from precursor pollutants emitted by 66 individual airports. We linked airport- and pollutant-specific concentrations with population data and literature-based concentration-response functions to create health damage functions. Deaths per 1000t of primary PM2.5 emissions ranged from 3 to 160 across airports, with variability explained by population patterns within 500km of the airport. Deaths per 1000t of precursors for secondary PM2.5 varied across airports from 0.1 to 2.7 for NOx, 0.06 to 2.9 for SO2, and 0.06 to 11 for VOCs, with variability explained by population patterns and ambient concentrations influencing particle formation. Deaths per 1000t of O3 precursors ranged from -0.004 to 1.0 for NOx and 0.03 to 1.5 for VOCs, with strong seasonality and influence of ambient concentrations. Our findings reinforce the importance of location- and source-specific health damage functions in design of health-maximizing emissions control policies.

Framework for assessing causality of air pollution-related health effects for reviews of the National Ambient Air Quality Standards.

To inform regulatory decisions on the risk due to exposure to ambient air pollution, consistent and transparent communication of the scientific evidence is essential. The United States Environmental Protection Agency (U.S. EPA) develops the Integrated Science Assessment (ISA), which contains evaluations of the policy-relevant science on the effects of criteria air pollutants and conveys critical science judgments to inform decisions on the National Ambient Air Quality Standards. This article discusses the approach and causal framework used in the ISAs to evaluate and integrate various lines of scientific evidence and draw conclusions about the causal nature of air pollution-induced health effects. The framework has been applied to diverse pollutants and cancer and noncancer effects. To demonstrate its flexibility, we provide examples of causality judgments on relationships between health effects and pollutant exposures, drawing from recent ISAs for ozone, lead, carbon monoxide, and oxides of nitrogen. U.S. EPA's causal framework has increased transparency by establishing a structured process for evaluating and integrating various lines of evidence and uniform approach for determining causality. The framework brings consistency and specificity to the conclusions in the ISA, and the flexibility of the framework makes it relevant for evaluations of evidence across media and health effects.