What doesn’t kill her,will make her depressed

In this paper we study the long run effects of the 1959–61 Chinese Famine on mental health outcomes. We focus on cohorts that were born during the famine and examine their mental health as adults, when they are roughly 55 years of age. We find that early-life exposure to this famine leads to a large statistically significant negative impact on women’s mental health, while there is limited effect on men. This gender differential effect is observed because male fetuses experience a stronger natural selection as compared to female fetuses, which implies that in the longer run, surviving females may exhibit larger detrimental effects of early-life famine exposure. Thus, the observed effects are a composite of two well-established factors, the survival of the fittest and the Fetal Origins hypothesis.     

Comparison of tobacco control scenarios: quantifying estimates of long-term health impact using the DYNAMO-HIA modeling tool

Background

There are several types of tobacco control interventions/policies which can change future smoking exposure. The most basic intervention types are 1) smoking cessation interventions 2) preventing smoking initiation and 3) implementation of a nationwide policy affecting quitters and starters simultaneously. The possibility for dynamic quantification of such different interventions is key for comparing the timing and size of their effects.

Methods and Results

We developed a software tool, DYNAMO-HIA, which allows for a quantitative comparison of the health impact of different policy scenarios. We illustrate the outcomes of the tool for the three typical types of tobacco control interventions if these were applied in the Netherlands. The tool was used to model the effects of different types of smoking interventions on future smoking prevalence and on health outcomes, comparing these three scenarios with the business-as-usual scenario. The necessary data input was obtained from the DYNAMO-HIA database which was assembled as part of this project. All smoking interventions will be effective in the long run. The population-wide strategy will be most effective in both the short and long term. The smoking cessation scenario will be second-most effective in the short run, though in the long run the smoking initiation scenario will become almost as effective. Interventions aimed at preventing the initiation of smoking need a long time horizon to become manifest in terms of health effects. The outcomes strongly depend on the groups targeted by the intervention.

Conclusion

We calculated how much more effective the population-wide strategy is, in both the short and long term, compared to quit smoking interventions and measures aimed at preventing the initiation of smoking. By allowing a great variety of user-specified choices, the DYNAMO-HIA tool is a powerful instrument by which the consequences of different tobacco control policies and interventions can be assessed.     

The effect of low birth weight on height,weight and behavioral outcomes in the medium-run

A number of studies have documented negative long term effects of low birth weight. Yet, not much is known about the dynamics of the process leading to adverse health and educational outcomes in the long run. While previous studies focusing mainly on LBW effects on physical growth and cognitive outcomes have found effects of the same size at both school age and young adulthood, others have found a diminishing negative effect over time. The purpose of this paper was to bring new evidence to this issue by analyzing the medium run effects of low birth weight on child behavioral outcomes as well as physical growth at ages 6 months, 3½, 7½ and 11 years using data from the Danish Longitudinal Survey of Children. Observing the same children at different points in time enabled us to chart the evolution of anthropometric and behavioral deficits among children born with low birth weight and helped understanding the nature and timing of interventions.     

Air pollution from natural and anthropic sources and male fertility

Exposure to air pollution has been clearly associated with a range of adverse health effects, including reproductive toxicity. However, a limited amount of research has been conducted to examine the association between air pollution and male reproductive outcomes, specially semen quality. We performed a systematic review (up to March 2017) to assess the impact of environmental and occupational exposure to air pollution on semen quality. Epidemiological studies focusing on air pollution exposures and male reproduction were identified by a search of the PUBMED, MEDLINE, EBSCO and TOXNET literature bases. Twenty-two studies were included which assess the impact of air pollutants (PM_2.5, PM₁₀, SO₂, NOx, O₃, PAHs) on main semen parameters (sperm concentration, motility, morphology), CASA parameters, DNA fragmentation, sperm aneuploidy and the level of reproductive hormones. The number of studies found significant results supporting the evidence that air pollution may affect: DNA fragmentation, morphology and motility.In summary, most studies concluded that outdoor air pollution affects at least one of the assessed semen parameters. However the diversity of air pollutants and semen parameters presented in the studies included in the review and different study design caused lack of consistency in results and difficulties in comparison.     

Quantifying the health impacts of air pollution under a changing climate—a review of approaches and methodology

Climate change has been predicted to affect future air quality, with inevitable consequences for health. Quantifying the health effects of air pollution under a changing climate is crucial to provide evidence for actions to safeguard future populations. In this paper, we review published methods for quantifying health impacts to identify optimal approaches and ways in which existing challenges facing this line of research can be addressed. Most studies have employed a simplified methodology, while only a few have reported sensitivity analyses to assess sources of uncertainty. The limited investigations that do exist suggest that examining the health risk estimates should particularly take into account the uncertainty associated with future air pollution emissions scenarios, concentration-response functions, and future population growth and age structures. Knowledge gaps identified for future research include future health impacts from extreme air pollution events, interactions between temperature and air pollution effects on public health under a changing climate, and how population adaptation and behavioural changes in a warmer climate may modify exposure to air pollution and health consequences.     

Impact of air pollution and climate change on mental health outcomes: an umbrella review of global evidence

The impact of air pollution and climate change on mental health has recently raised strong concerns. However, a comprehensive overview analyzing the existing evidence while addressing relevant biases is lacking. This umbrella review systematically searched the PubMed/Medline, Scopus and PsycINFO databases (up to June 26, 2023) for any systematic review with meta-analysis investigating the association of air pollution or climate change with mental health outcomes. We used the R metaumbrella package to calculate and stratify the credibility of the evidence according to criteria (i.e., convincing, highly suggestive, suggestive, or weak) that address several biases, complemented by sensitivity analyses. We included 32 systematic reviews with meta-analysis that examined 284 individual studies and 237 associations of exposures to air pollution or climate change hazards and mental health outcomes. Most associations (n=195, 82.3%) involved air pollution, while the rest (n=42, 17.7%) regarded climate change hazards (mostly focusing on temperature: n=35, 14.8%). Mental health outcomes in most associations (n=185, 78.1%) involved mental disorders, followed by suicidal behavior (n=29, 12.4%), access to mental health care services (n=9, 3.7%), mental disorders-related symptomatology (n=8, 3.3%), and multiple categories together (n=6, 2.5%). Twelve associations (5.0%) achieved convincing (class I) or highly suggestive (class II) evidence. Regarding exposures to air pollution, there was convincing (class I) evidence for the association between long-term exposure to solvents and a higher incidence of dementia or cognitive impairment (odds ratio, OR=1.139), and highly suggestive (class II) evidence for the association between long-term exposure to some pollutants and higher risk for cognitive disorders (higher incidence of dementia with high vs. low levels of carbon monoxide, CO: OR=1.587; higher incidence of vascular dementia per 1 μg/m³ increase of nitrogen oxides, NO_x: hazard ratio, HR=1.004). There was also highly suggestive (class II) evidence for the association between exposure to airborne particulate matter with diameter ≤10 μm (PM₁₀) during the second trimester of pregnancy and the incidence of post-partum depression (OR=1.023 per 1 μg/m³ increase); and for the association between short-term exposure to sulfur dioxide (SO₂) and schizophrenia relapse (risk ratio, RR=1.005 and 1.004 per 1 μg/m³ increase, respectively 5 and 7 days after exposure). Regarding climate change hazards, there was highly suggestive (class II) evidence for the association between short-term exposure to increased temperature and suicide- or mental disorders-related mortality (RR=1.024), suicidal behavior (RR=1.012), and hospital access (i.e., hospitalization or emergency department visits) due to suicidal behavior or mental disorders (RR=1.011) or mental disorders only (RR=1.009) (RR values per 1°C increase). There was also highly suggestive (class II) evidence for the association between short-term exposure to increased apparent temperature (i.e., the temperature equivalent perceived by humans) and suicidal behavior (RR=1.01 per 1°C increase). Finally, there was highly suggestive (class II) evidence for the association between the temporal proximity of cyclone exposure and severity of symptoms of post-traumatic stress disorder (r=0.275). Although most of the above associations were small in magnitude, they extend to the entire world population, and are therefore likely to have a substantial impact. This umbrella review classifies and quantifies for the first time the global negative impacts that air pollution and climate change can exert on mental health, identifying evidence-based targets that can inform future research and population health actions.     

Adverse reproductive outcomes from exposure to environmental mutagens.

The effect of environmental pollution on reproductive outcomes has been studied in the research project 'Teplice Program' analyzing the impact of air pollution on human health. Genotoxicity of urban air particles <10 microm (PM10) in in vitro system was determined by the analysis of DNA adducts. The highest DNA binding activity was observed in aromatic fraction, identifying DNA adducts of carcinogenic polycyclic aromatic hydrocarbons (PAHs) presumably diolepoxide-derived from: 9-hydroxybenzo[a]pyrene (9-OH-B[a]P), benzo[a]pyrene-r-7,-dihydrodiol-t-9,10-epoxide[+] (anti-BPDE), benzo[b]fluoranthene (B[b]F), chrysene (CHRY), benz[a]antracene (B[a]A), indeno[1,2,3-cd]pyrene (I[cd]P). Reproductive studies were conducted in both females and males. A study of the effects of PM10 exposure on pregnancy outcomes found the relationship between the intrauterine growth retardation (IUGR) and PM10 levels over 40 microg/m(3) in the first gestational month (Odds Ratio for 40-50 microg/m(3)50 microg/m(3)=1.9). Selected biomarkers were analyzed in venous blood, cord blood (chromosomal aberrations, comet assay) and placenta (DNA adducts, genetic polymorphisms of GSTM1 and NAT2 genotypes) of women enrolled in a nested case-control study. DNA adduct levels were higher in polluted vs. control districts, in smoking vs. nonsmoking mothers, and in GSTM1 null genotype, which was more pronounced in polluted district. No effect of air pollution was observed by cytogenetic analysis of chromosomal aberrations or by comet assay. The reproductive development of young men was followed by measures of semen quality, adjusted for ambient SO(2) exposure. The analysis identified significant associations with air pollution for <13% morphologically normal sperm, <29% sperm with normal head shape, <24% motile sperm. Analysis of aneuploidy in human sperm by FISH showed, aneuploidy YY8 was associated with season of heaviest air pollution. These findings are suggestive for an influence of air pollution on YY8 disomy. All these results indicate that air pollution may increase DNA damage in human population, which may be even higher for susceptible groups. Biomarkers of exposure (DNA adducts) and susceptibility (GSTM1 and NAT2) may indicate the risk of presumable low environmental exposure. Pregnancy outcome and semen studies imply that relatively low air pollution (higher than 40 microg PM10/m(3)) can significantly increase the adverse reproductive outcomes affecting both genders.     

Particulate urban air pollution affects the functional morphology of mouse placenta

In humans, adverse pregnancy outcomes (low birth weight, prematurity, and intrauterine growth retardation) are associated with exposure to urban air pollution. Experimental data have also shown that such exposure elicits adverse reproductive outcomes. We hypothesized that the effects of urban air pollution on pregnancy outcomes could be related to changes in functional morphology of the placenta. To test this, future dams were exposed during pregestational and gestational periods to filtered or nonfiltered air in exposure chambers. Placentas were collected from near-term pregnancies and prepared for microscopical examination. Fields of view on vertical uniform random tissue slices were analyzed using stereological methods. Volumes of placental compartments were estimated, and the labyrinth was analyzed further in terms of its maternal vascular spaces, fetal capillaries, trophoblast, and exchange surface areas. From these primary data, secondary quantities were derived: vessel calibers (expressed as diameters), trophoblast thickness (arithmetic mean), and total and mass-specific morphometric diffusive conductances for oxygen of the intervascular barrier. Two-way analysis of variance showed that both periods of exposure led to significantly smaller fetal weights. Pregestational exposure to nonfiltered air led to significant increases in fetal capillary surface area and in total and mass-specific conductances. However, the calibers of maternal blood spaces were reduced. Gestational exposure to nonfiltered air was associated with reduced volumes, calibers, and surface areas of maternal blood spaces and with greater fetal capillary surfaces and diffusive conductances. The findings indicate that urban air pollution affects placental functional morphology. Fetal weights are compromised despite attempts to improve diffusive transport across the placenta.     

A measurement error model for time-series studies of air pollution and mortality

One barrier to interpreting the observational evidence concerning the adverse health effects of air pollution for public policy purposes is the measurement error inherent in estimates of exposure based on ambient pollutant monitors. Exposure assessment studies have shown that data from monitors at central sites may not adequately represent personal exposure. Thus, the exposure error resulting from using centrally measured data as a surrogate for personal exposure can potentially lead to a bias in estimates of the health effects of air pollution. This paper develops a multi-stage Poisson regression model for evaluating the effects of exposure measurement error on estimates of effects of particulate air pollution on mortality in time-series studies. To implement the model, we have used five validation data sets on personal exposure to PM10. Our goal is to combine data on the associations between ambient concentrations of particulate matter and mortality for a specific location, with the validation data on the association between ambient and personal concentrations of particulate matter at the locations where data have been collected. We use these data in a model to estimate the relative risk of mortality associated with estimated personal-exposure concentrations and make a comparison with the risk of mortality estimated with measurements of ambient concentration alone. We apply this method to data comprising daily mortality counts, ambient concentrations of PM10measured at a central site, and temperature for Baltimore, Maryland from 1987 to 1994. We have selected our home city of Baltimore to illustrate the method; the measurement error correction model is general and can be applied to other appropriate locations.Our approach uses a combination of: (1) a generalized additive model with log link and Poisson error for the mortality-personal-exposure association; (2) a multi-stage linear model to estimate the variability across the five validation data sets in the personal-ambient-exposure association; (3) data augmentation methods to address the uncertainty resulting from the missing personal exposure time series in Baltimore. In the Poisson regression model, we account for smooth seasonal and annual trends in mortality using smoothing splines. Taking into account the heterogeneity across locations in the personal-ambient-exposure relationship, we quantify the degree to which the exposure measurement error biases the results toward the null hypothesis of no effect, and estimate the loss of precision in the estimated health effects due to indirectly estimating personal exposures from ambient measurements.     

Negative Life Events Vary by Neighborhood and Mediate the Relation between Neighborhood Context and Psychological Well-Being

Researchers have speculated that negative life events are more common in troubled neighborhoods, amplifying adverse effects on health. Using a clustered representative sample of Chicago residents (2001–03; n = 3,105) from the Chicago Community Adult Health Survey, we provide the first documentation that negative life events are highly geographically clustered compared to health outcomes. Associations between neighborhood context and negative life events were also found to vary by event type. We then demonstrate the power of a contextualized approach by testing path models in which life events mediate the relation between neighborhood characteristics and health outcomes, including self-rated health, anxiety, and depression. The indirect paths between neighborhood conditions and health through negative life event exposure are highly significant and large compared to the direct paths from neighborhood conditions to health. Our results indicate that neighborhood conditions can have acute as well as chronic effects on health, and that negative life events are a powerful mechanism by which context may influence health.     

An informative Bayesian structural equation model to assess source-specific health effects of air pollution

A primary objective of current air pollution research is the assessment of health effects related to specific sources of air particles or particulate matter (PM). Quantifying source-specific risk is a challenge because most PM health studies do not directly observe the contributions of the pollution sources themselves. Instead, given knowledge of the chemical characteristics of known sources, investigators infer pollution source contributions via a source apportionment or multivariate receptor analysis applied to a large number of observed elemental concentrations. Although source apportionment methods are well established for exposure assessment, little work has been done to evaluate the appropriateness of characterizing unobservable sources thus in health effects analyses. In this article, we propose a structural equation framework to assess source-specific health effects using speciated elemental data. This approach corresponds to fitting a receptor model and the health outcome model jointly, such that inferences on the health effects account for the fact that uncertainty is associated with the source contributions. Since the structural equation model (SEM) typically involves a large number of parameters, for small-sample settings, we propose a fully Bayesian estimation approach that leverages historical exposure data from previous related exposure studies. We compare via simulation the performance of our approach in estimating source-specific health effects to that of 2 existing approaches, a tracer approach and a 2-stage approach. Simulation results suggest that the proposed informative Bayesian SEM is effective in eliminating the bias incurred by the 2 existing approaches, even when the number of exposures is limited. We employ the proposed methods in the analysis of a concentrator study investigating the association between ST-segment, a cardiovascular outcome, and major sources of Boston PM and discuss the implications of our findings with respect to the design of future PM concentrator studies.     

Non-cancer effects of chemical agents on children's health

This paper provides an overview about the non-cancer health effects for children from relevant chemical agents in our environment. In addition, a meta-analysis was conducted on the association between sudden infant death syndrome (SIDS) and maternal smoking during pregnancy as well as postnatal exposure to environmental tobacco smoke (ETS).In children, birth deformities, neurodevelopment, reproductive outcomes and respiratory system are mainly affected by chemical exposures. According to recent systematic reviews, evidence is sufficient for cognitive impairments caused by low lead exposure levels. Evidence for neurotoxicity from prenatal methylmercury exposure is sufficient for high exposure levels and limited for low levels. Prenatal exposure to polychlorinated biphenyls (PCB) and related toxicants results in cognitive and motor deficits.Maternal smoking during pregnancy is a risk factor for preterm birth, foetal growth deficit and SIDS. The meta-analytic pooled risk estimate for SIDS based on 15 studies is 2.94 (95% confidence interval: 2.43–3.57). Postnatal exposure to ETS was found to increase the SIDS risk by a factor of 1.72 (95% CI: 1.28–2.30) based on six studies which took into account maternal smoking during pregnancy. Additionally, postnatal ETS exposure causes acute respiratory infections, ear problems, respiratory symptoms, more severe asthma, and it slows lung growth. These health effects are also of concern for postnatal exposure to ambient and indoor air pollution.Children differ from adults with respect to several aspects which are relevant for assessing their health risk. Thus, independent evaluation of toxicity in childhood populations is essential.     

Genomic damage in children accidentally exposed to ionizing radiation: a review of the literature

During the last decade, our knowledge of the mechanisms by which children respond to exposures to physical and chemical agents present in the environment, has significantly increased. Results of recent projects and programmes focused on children's health underline a specific vulnerability of children to environmental genotoxicants. Environmental research on children predominantly investigates the health effects of air pollution while effects from radiation exposure deserve more attention. The main sources of knowledge on genome damage of children exposed to radiation are studies performed after the Chernobyl nuclear plant accident in 1986. The present review presents and discusses data collected from papers analyzing genome damage in children environmentally exposed to ionizing radiation. Overall, the evidence from the studies conducted following the Chernobyl accident, nuclear tests, environmental radiation pollution and indoor accidental contamination reveals consistently increased chromosome aberration and micronuclei frequency in exposed than in referent children. Future research in this area should be focused on studies providing information on: (a) effects on children caused by low doses of radiation; (b) effects on children from combined exposure to low doses of radiation and chemical agents from food, water and air; and (c) specific effects from exposure during early childhood (radioisotopes from water, radon in homes). Special consideration should also be given to a possible impact of a radiochemical environment to the development of an adaptive response for genomic damage. Interactive databases should be developed to provide integration of cytogenetic data, childhood cancer registry data and information on environmental contamination. The overall aim is to introduce timely and efficient preventive measures, by means of a better knowledge of the early and delayed health effects in children resulting from radiation exposure.     

Air pollution and the lung: epidemiological approach

Epidemiological evidence has concurred with clinical and experimental evidence to correlate current levels of ambient air pollution, both indoors and outdoors, with respiratory effects. In this respect, the use of specific epidemiological methods has been crucial. Common outdoor pollutants are particulate matter, nitrogen dioxide, carbon monoxide, volatile organic compounds and ozone. Short-term effects of outdoor air pollution include changes in lung function, respiratory symptoms and mortality due to respiratory causes. Increase in the use of health care resources has also been associated with short-term effects of air pollution. Long-term effects of cumulated exposure to urban air pollution include lung growth impairment, chronic obstructive pulmonary disease (COPD), lung cancer, and probably the development of asthma and allergies. Lung cancer and COPD have been related to a shorter life expectancy. Common indoor pollutants are environmental tobacco smoke, particulate matter, nitrogen dioxide, carbon monoxide, volatile organic compounds and biological allergens. Concentrations of these pollutants can be many times higher indoors than outdoors. Indoor air pollution may increase the risk of irritation phenomena, allergic sensitisation, acute and chronic respiratory disorders and lung function impairment. Recent conservative estimates have shown that 1.5-2 million deaths per year worldwide could be attributed to indoor air pollution. Further epidemiological research is necessary to better evaluate the respiratory health effects of air pollution and to implement protective programmes for public health.     

Estimating Mortality Derived from Indoor Exposure to Particles of Outdoor Origin

Following an extensive review of the literature, we further analyze the published data to examine the health effects of indoor exposure to particulate matter (PM) of outdoor origin. We obtained data on all-cause, cardiovascular, and respiratory mortality per 10 μg/m³ increase in outdoor PM₁₀ or PM_2.5; the infiltration factors for buildings; and estimated time spent outdoors by individuals in the United States, Europe, China, and globally. These data were combined log-linear exposure–response model to estimate the all-cause, cardiovascular, and respiratory mortality of exposure to indoor PM pollution of outdoor origin. Indoor PM pollution of outdoor origin is a cause of considerable mortality, accounting for 81% to 89% of the total increase in mortality associated with exposure to outdoor PM pollution for the studied regions. The findings suggest that enhancing the capacity of buildings to protect occupants against exposure to outdoor PM pollution has significant potential to improve public health outcomes.     

Effects of air pollution and habitual exercise on the risk of death: a longitudinal cohort study

Background:Exercise may exacerbate the adverse health effects of air pollution by increasing the inhalation of air pollutants. We investigated the combined effects of long-term exposure to fine particle matter (PM_2.5) and habitual exercise on deaths from natural causes in Taiwan.Methods:We recruited 384 130 adults (aged ≥ 18 yr) with 842 394 medical examination records between 2001 and 2016, and followed all participants until May 31, 2019. We obtained vital data from the National Death Registry of Taiwan. We estimated PM_2.5 exposure using a satellite-based spatiotemporal model, and collected information on exercise habits using a standard self-administered questionnaire. We analyzed the data using a Cox regression model with time-dependent covariates.Results:A higher level of habitual exercise was associated with a lower risk of death from natural causes, compared with inactivity (hazard ratio [HR] 0.84, 95% confidence interval [CI] 0.80–0.88 for the moderate exercise group; HR 0.65, 95% CI 0.62–0.68 for the high exercise groups), whereas a higher PM_2.5 exposure was associated with a higher risk of death from natural causes compared with lower exposure (HR 1.02, 95% CI 0.98–1.07, and HR 1.15, 95% CI 1.10–1.20, for the moderate and high PM_2.5 exposure groups, respectively). Compared with inactive adults with high PM_2.5 exposure, adults with high levels of habitual exercise and low PM_2.5 exposure had a substantially lower risk of death from natural causes. We found a minor, but statistically significant, interaction effect between exercise and PM_2.5 exposure on risk of death (HR 1.03 95% CI 1.01–1.06). Subgroup analyses, stratified by PM_2.5 categories, suggested that moderate and high levels of exercise were associated with a lower risk of death in each PM_2.5 stratum, compared with inactivity.Interpretation:Increased levels of exercise and reduced PM_2.5 exposure are associated with a lower risk of death from natural causes. Habitual exercise can reduce risk regardless of the levels of PM_2.5 exposure. Our results suggest that exercise is a safe health improvement strategy, even for people residing in relatively polluted regions.

Air pollution and physical inactivity are both major public health challenges worldwide.¹ Air pollution was the fifth leading cause of disability related to health and accounted for 4.9 million deaths worldwide in 2017.² More than 91% of the global population lives in areas where air quality does not meet the World Health Organization (WHO) guidelines.³ In addition, physical inactivity was the fourth leading risk factor for death globally, accounting for 5.3 million deaths worldwide in 2012.⁴ The WHO has challenged its member states to reduce physical inactivity by 15% by 2030.⁵As people exercise, their ventilation rate increases, which increases the volume of air pollutants they inhale. This may exacerbate the adverse health effects of air pollutants. Thus, the risk–benefit relation between air pollution and exercise needs to be assessed to understand whether it is safe to exercise regularly in polluted regions. Indeed, some studies have shown that acute exposure to air pollution when exercising may override the benefits of exercise.^6,7 It is possible that the effects of long-term exposure to air pollution may be irreversible and cause a much larger disease burden than short-term exposure. Limited information exists on the combined effects of long-term exposure to air pollution and habitual exercise on human health, and findings have been inconsistent depending on health outcome. Three cohort studies have explored the relation between air pollution, physical activity and risk of death in Hong Kong,⁸ Denmark and the United States,⁹ with relatively small sample sizes.¹⁰ Therefore, we sought to investigate the combined effects of habitual exercise and long-term exposure to fine particle matter (PM_2.5) on the risk of death from natural causes (i.e., deaths not attributable to accident, suicide or homicide) using a longitudinal cohort of adults in Taiwan, where the annual PM_2.5 concentrations are 1.6 times higher than the WHO-recommended limit. We hypothesized that the beneficial effects of habitual exercise on risk of death may outweigh the risk of high levels of air pollutants inhaled during exercise.     

Selective mortality and fertility and long run health effects of prenatal wartime exposure

Many previous studies have shown that prenatal exposure to adverse historical circumstances negatively affects long-run health. Most women who are pregnant during wars experience clearly adverse circumstances that are however not as harsh as the typically studied extreme episodes such as famines, combat and wide-scale destruction. We show that prenatal exposure to World War II (WWII) in five Western European countries did not lead to a population-wide poorer health among the elderly. We even find indications of a better than expected health. This is likely due to selective fertility and mortality. We attempt to quantify these selection effects and show that when taking them into account, the initially positively estimated health effects on almost all outcomes are substantially attenuated. Selective mortality and fertility likely occur in similar directions for many historical episodes of adversity. Our results therefore suggest that a part of the previous research on such exposures likely under estimated the true sizes of the long-run effects.     

MicroRNAs as biomarkers of harmful environmental and occupational exposures: a systematic review

Abstract

Environmental exposure is a growing public health burden associated with several negative health effects. An estimated 4.2 million deaths occur each year from ambient air pollution alone. Biomarkers that reflect specific exposures have the potential to measure the real integrated internal dose from all routes of complex environmental exposure. MicroRNAs (miRNAs), small non-coding RNAs that regulate gene expression, have been studied as biomarkers in various diseases and have also shown potential as environmental exposure biomarkers. Here, we review the available human epidemiological and experimental evidence of miRNA expression changes in response to specific environmental exposures including airborne particulate matter. In doing so, we establish that miRNA exposure biomarker development remains in its infancy and future studies will need to carefully consider biological and analytical ‘design rules’ in order to facilitate clinical translation.     

A Historical Overview of the Ozone Exposure Problem

Ozone can be found in essentially all locations in the troposphere. Too much exposure of vegetation and humans to this potent oxidizing gas can prove toxic. Reports of human toxicity to ozone first appeared in the 1800's from accidental occupational exposures when ozone was first discovered. Ozone was recognized as damaging field vegetation with a report of altered leaf morphology in grapes in the 1950s. Ozone is the major oxidant component in photochemical smog, and is produced by reactions of volatile organic compounds and oxides of nitrogen with sunlight present. Soon after the inception of the U.S. Environmental Protection Agency (US EPA), the Agency set a general “oxidants” standard (which included ozone) in 1971. A primary standard was created to protect human health and a secondary standard to protect against agricultural losses, ecological damage, and other losses. Ozone concentrations have decreased steadily over the last two decades in some areas of the U.S., but have increased in other areas. Several aspects of ozone exposure need further characterization, including better determination of rural concentrations and the relationship of outdoor to indoor concentrations. Ozone is one of the six criteria air pollutants requiring a formal reexamination of the new findings of effects on health and vegetation on a periodic basis, a process that leads to the publication of an US EPA criteria document. As a result of further study concerning ozone effects, significant changes were made to pollution standards in 1979 and 1997. This toxicant has remained a major air pollutant of concern in the U.S. despite regulation and intense study over several decades.     

Estimating causal effects of air quality regulations using principal stratification for spatially correlated multivariate intermediate outcomes

Methods for causal inference regarding health effects of air quality regulations are met with unique challenges because (1) changes in air quality are intermediates on the causal pathway between regulation and health, (2) regulations typically affect multiple pollutants on the causal pathway towards health, and (3) regulating a given location can affect pollution at other locations, that is, there is interference between observations. We propose a principal stratification method designed to examine causal effects of a regulation on health that are and are not associated with causal effects of the regulation on air quality. A novel feature of our approach is the accommodation of a continuously scaled multivariate intermediate response vector representing multiple pollutants. Furthermore, we use a spatial hierarchical model for potential pollution concentrations and ultimately use estimates from this model to assess validity of assumptions regarding interference. We apply our method to estimate causal effects of the 1990 Clean Air Act Amendments among approximately 7 million Medicare enrollees living within 6 miles of a pollution monitor.