Related Articles

Objective

There is growing interest in disentangling the health effects of spatially clustered social and physical environmental exposures and in exploring potential synergies among them, with particular attention directed to the combined effects of psychosocial stress and air pollution. Both exposures may be elevated in lower-income urban communities, and it has been hypothesized that stress, which can influence immune function and susceptibility, may potentiate the effects of air pollution in respiratory disease onset and exacerbation. In this paper, we attempt to synthesize the relevant research from social and environmental epidemiology, toxicology, immunology, and exposure assessment to provide a useful framework for environmental health researchers aiming to investigate the health effects of environmental pollution in combination with social or psychological factors.

Data synthesis

We review the existing epidemiologic and toxicologic evidence on synergistic effects of stress and pollution, and then describe the physiologic effects of stress and key issues related to measuring and evaluating stress as it relates to physical environmental exposures and susceptibility. Finally, we identify some of the major methodologic challenges ahead as we work toward disentangling the health effects of clustered social and physical exposures and accurately describing the interplay among these exposures.

Conclusions

There is still tremendous work to be done toward understanding the combined and potentially synergistic health effects of stress and pollution. As this research proceeds, we recommend careful attention to the relative temporalities of stress and pollution exposures, to nonlinearities in their independent and combined effects, to physiologic pathways not elucidated by epidemiologic methods, and to the relative spatial distributions of social and physical exposures at multiple geographic scales.

The influence of physical housing quality on childhood asthma expression, especially the effect of exposure to moulds, allergens, and pollutants, is well documented. However, attempts to explain increasing rates and severity of childhood asthma solely through physical environmental factors have been unsuccessful, and additional exposures may be involved. Increasing evidence has linked psychological stress and negative affective states to asthma expression. At the same time, recent scholarship in the social sciences has focused on understanding how social environments, such as housing, “get under the skin” to influence health, and suggests that psychological factors play a key role. While there is relevant overlapping research in social science, psychology, economics, and health policy in this area, findings from these disciplines have not yet been conceptually integrated into ongoing asthma research. We propose to expand the dimensions of housing considered in future asthma research to include both physical and psychological aspects which may directly and indirectly influence onset and severity of disease expression. This synthesis of overlapping research from a number of disciplines argues for the systematic measure of psychological dimensions of housing and consideration of the interplay between housing stress and physical housing characteristics in relation to childhood asthma.

Perceived risk of environmental threats often translates into psychological stress with a wide range of effects on health and well-being. Petrochemical industrial complexes constitute one of the sites that can cause considerable pollution and health problems. The uncertainty around emissions results in a perception of risk for citizens residing in neighboring areas, which translates into anxiety and physiological stress. In this context, social trust is a key factor in managing the perceived risk. In the case of industrial risks, it is essential to distinguish between trust in the companies that make up the industry, and trust in public institutions. In the context of a petrochemical industrial complex located in the port of Castellón (Spain), this paper primarily discusses how trust—both in the companies located in the petrochemical complex and in the public institutions—affects citizens’ health risk perception. The research findings confirm that while the trust in companies negatively affects citizens’ health risk perception, trust in public institutions does not exert a direct and significant effect. Analysis also revealed that trust in public institutions and health risk perception are essentially linked indirectly (through trust in companies).

Background

Disproportionate life stress and consequent physiologic alteration (i.e., immune dysregulation) has been proposed as a major pathway linking socioeconomic position, environmental exposures, and health disparities. Asthma, for example, disproportionately affects lower-income urban communities, where air pollution and social stressors may be elevated.

Objectives

We aimed to examine the role of exposure to violence (ETV), as a chronic stressor, in altering susceptibility to traffic-related air pollution in asthma etiology.

Methods

We developed geographic information systems (GIS)–based models to retrospectively estimate residential exposures to traffic-related pollution for 413 children in a community-based pregnancy cohort, recruited in East Boston, Massachusetts, between 1987 and 1993, using monthly nitrogen dioxide measurements for 13 sites over 18 years. We merged pollution estimates with questionnaire data on lifetime ETV and examined the effects of both on childhood asthma etiology.

Results

Correcting for potential confounders, we found an elevated risk of asthma with a 1-SD (4.3 ppb) increase in NO2 exposure solely among children with above-median ETV [odds ratio (OR) = 1.63; 95% confidence interval (CI), 1.14–2.33)]. Among children always living in the same community, with lesser exposure measurement error, this association was magnified (OR = 2.40; 95% CI, 1.48–3.88). Of multiple exposure periods, year-of-diagnosis NO2 was most predictive of asthma outcomes.

Conclusions

We found an association between traffic-related air pollution and asthma solely among urban children exposed to violence. Future studies should consider socially patterned susceptibility, common spatial distributions of social and physical environmental factors, and potential synergies among these. Prospective assessment of physical and social exposures may help determine causal pathways and critical exposure periods.

Individuals exposed to psychological stressors may experience a long-term resetting of behavioral and neuroendocrine aspects of their “stress response” so that they either hyper or hypo-respond to subsequent stressors. These effects of psychological or traumatic stressors may be mimicked in rats using the resident-intruder model of social defeat.

The social defeat model has been characterized to model aspects of the physiology and behavior associated with anxiety and depression. The objective of this study was to determine if behaviors elicited following repeated social defeat can also reflect aspects of ethologically relevant stresses associated with existing post traumatic stress disorder (PTSD) models. Socially defeated rats displayed weight loss and an enhanced and prolonged response to acoustic startle which was displayed for up to 10 days following repeated social defeat. These data indicate that the severe stress of social defeat can produce physiologic and behavioral outcomes which may reflect aspects of traumatic psychosocial stress.

Conventionally, in its decision-making, the U.S. EPA has evaluated the effects and risks associated with a single pollutant in a single exposure medium. In reality, people are exposed to mixtures of pollutants or to the same pollutant through a variety of media, including the air, water, and food. It is now more recognized than before that environmental exposure to pollutants occurs via multiple exposure routes and pathways, including inhalation, ingestion, and dermal absorption. Moreover, chemical, biologic, radiologic, physical, and psychologic stressors are all acknowledged as affecting human health. Although many EPA offices attempt to consider cumulative risk assessment and cumulative effects in various ways, there is no Agency-wide policy for considering these risks and the effects of exposure to these risks when making environmental decisions. This article examines how U.S. courts might assess EPA’s general authority and discretion to use cumulative risk assessment as the basis for developing data in support of environmental decision-making, and how courts might assess the validity of a cumulative risk assessment methodology itself.

Psychological attitudes are prospectively related to cardiovascular disease (CVD), but a causal relationship has not been demonstrated. Trait optimism/pessimism (positive or negative future expectation, respectively), and cynical hostility (mistrust of people), are attitudes with features of personality traits. These attitudes may affect CVD risk in several ways, by influencing an individual’s 1) adoption of health behaviors, 2) maladaptive stress responding resulting in direct alteration of physiology (i.e., autonomic dysfunction, thrombosis, arrhythmias), 3) development of traditional CVD risk factors, and 4) lack of adherence to therapy in both primary and secondary prevention. More adaptive attitudes may favorably influence CVD risk at each of these critical junctures. The genetic and environmental (i.e., social, economic, racial/ethnic) determinants of attitudes have not been extensively studied. In addition, it is important to understand how some of these environmental determinants may also moderate the association between attitudes and CVD. Clinical trials to modify attitudes for CVD risk reduction (either by reducing negative attitudes or by increasing positive attitudes) are difficult to conduct, but are necessary to determine whether attitudes can indeed be modified, and if, so, to quantify any CVD-related benefits. To address these questions we present a broad, multidisciplinary research agenda utilizing mixed methods and integrating principles of epidemiology, genetics, psychophysiology, and behavioral medicine over the lifecourse (Figure 1). This overview focuses on attitudes and CVD, but has broader implications for understanding how psychological factors relate to chronic diseases of adulthood.

Recent results suggest that adverse health effects of air pollution exist at levels of pollutants around or even below air quality standards set by national and international institutions. Furthermore, there are indications that air pollution effects on health may be partly determined by specific mixtures of air pollutants and may be altered by other environmental, behavioral, and social patterns. Southern European countries share some common characteristics in terms of climate, geography, and life activity patterns. Results from studies undertaken in France, Greece, Italy, Portugal, and Spain investigating short- and long-term air pollution health effects are presented and their consistency demonstrated. These results provide adequate evidence that health effects--particularly short-term--of the currently measured urban air pollution levels exist. However, information available so far does not allow an assessment of regional differences in the health effects of air pollution as far as the Mediterranean region of Europe is concerned. It is suggested that the interaction between the traditional pollution (mainly characterized by high levels of black smoke and SO2) and photochemical pollution must be investigated in this area, as well as the possible interaction between air pollution and high temperature and other meteorologic factors. In addition, measurements of individual exposure to different pollutants, affected by the pollutant's levels in specific micro-environments and the individual's time-activity pattern, must be undertaken for a better understanding of the air pollution-health link. Finally, the importance of the reported air pollution health effects in terms of public health must be addressed more closely.

Background

Environmental changes, air pollution and ozone depletion are increasing oxidative stress, and global warming threatens health by heat stress. We now face a high risk of simultaneous exposure to heat and oxidative stress. However, there have been few studies investigating their combined adverse effects on cell viability.

Principal Findings

Pretreatment of hydrogen peroxide (H2O2) specifically and highly sensitized cells to heat stress, and enhanced loss of mitochondrial membrane potential. H2O2 exposure impaired the HSP40/HSP70 induction as heat shock response (HSR) and the unfolded protein recovery, and enhanced eIF2α phosphorylation and/or XBP1 splicing, land marks of ER stress. These H2O2-mediated effects mimicked enhanced heat sensitivity in HSF1 knockdown or knockout cells. Importantly, thermal preconditioning blocked H2O2–mediated inhibitory effects on refolding activity and rescued HSF1 +/+ MEFs, but neither blocked the effects nor rescued HSF1 -/- MEFs. These data strongly suggest that inhibition of HSR and refolding activity is crucial for H2O2–mediated enhanced heat sensitivity.

Conclusions

H2O2 blocks HSR and refolding activity under heat stress, thereby leading to insufficient quality control and enhancing ER stress. These uncontrolled stress responses may enhance cell death. Our data thus highlight oxidative stress as a crucial factor affecting heat tolerance.

Human skin is constantly directly exposed to the air, solar radiation, environmental pollutants, or other mechanical and chemical insults, which are capable of inducing the generation of free radicals as well as reactive oxygen species (ROS) of our own metabolism. Extrinsic skin damage develops due to several factors: ionizing radiation, severe physical and psychological stress, alcohol intake, poor nutrition, overeating, environmental pollution, and exposure to UV radiation (UVR). It is estimated that among all these environmental factors, UVR contributes up to 80%. UV-induced generation of ROS in the skin develops oxidative stress, when their formation exceeds the antioxidant defence ability of the target cell. The primary mechanism by which UVR initiates molecular responses in human skin is via photochemical generation of ROS mainly formation of superoxide anion (O2−∙), hydrogen peroxide (H2O2), hydroxyl radical (OH∙), and singlet oxygen (1O2). The only protection of our skin is in its endogenous protection (melanin and enzymatic antioxidants) and antioxidants we consume from the food (vitamin A, C, E, etc.). The most important strategy to reduce the risk of sun UVR damage is to avoid the sun exposure and the use of sunscreens. The next step is the use of exogenous antioxidants orally or by topical application and interventions in preventing oxidative stress and in enhanced DNA repair.

It is generally agreed that social ties play a beneficial role in the maintenance of psychological well-being. In this targeted review, we highlight four sets of insights that emerge from the literature on social ties and mental health outcomes (defined as stress reactions, psychological well-being, and psychological distress, including depressive symptoms and anxiety). First, the pathways by which social networks and social supports influence mental health can be described by two alternative (although not mutually exclusive) causal models—the main effect model and the stress-buffering model. Second, the protective effects of social ties on mental health are not uniform across groups in society. Gender differences in support derived from social network participation may partly account for the higher prevalence of psychological distress among women compared to men. Social connections may paradoxically increase levels of mental illness symptoms among women with low resources, especially if such connections entail role strain associated with obligations to provide social support to others. Third, egocentric networks are nested within a broader structure of social relationships. The notion of social capital embraces the embeddedness of individual social ties within the broader social structure. Fourth, despite some successes reported in social support interventions to enhance mental health, further work is needed to deepen our understanding of the design, timing, and dose of interventions that work, as well as the characteristics of individuals who benefit the most.

Every year more than 13 million deaths worldwide are due to environmental pollutants, and approximately 24% of diseases are caused by environmental exposures that might be averted through preventive measures. Rapidly growing evidence has linked environmental pollutants with epigenetic variations, including changes in DNA methylation, histone modifications and microRNAs.

Environ mental chemicals and epigenetic changes All of these mechanisms are likely to play important roles in disease aetiology, and their modifications due to environmental pollutants might provide further understanding of disease aetiology, as well as biomarkers reflecting exposures to environmental pollutants and/or predicting the risk of future disease. We summarize the findings on epigenetic alterations related to environmental chemical exposures, and propose mechanisms of action by means of which the exposures may cause such epigenetic changes. We discuss opportunities, challenges and future directions for future epidemiology research in environmental epigenomics. Future investigations are needed to solve methodological and practical challenges, including uncertainties about stability over time of epigenomic changes induced by the environment, tissue specificity of epigenetic alterations, validation of laboratory methods, and adaptation of bioinformatic and biostatistical methods to high-throughput epigenomics. In addition, there are numerous reports of epigenetic modifications arising following exposure to environmental toxicants, but most have not been directly linked to disease endpoints. To complete our discussion, we also briefly summarize the diseases that have been linked to environmental chemicals-related epigenetic changes.

Social relationships are a fundamental aspect of life, affecting social, psychological, physiological, and behavioral functions. While social interactions can attenuate stress and promote health, disruption, confrontations, isolation, or neglect in the social environment can each be major stressors. Social stress can impair the basal function and stress-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis, impairing function of multiple biological systems and posing a risk to mental and physical health. In contrast, social support can ameliorate stress-induced physiological and immunological deficits, reducing the risk of subsequent psychological distress and improving an individual's overall well-being. For better clinical treatment of these physiological and mental pathologies, it is necessary to understand the regulatory mechanisms of stress-induced pathologies as well as determine the underlying biological mechanisms that regulate social buffering of the stress system. A number of ethologically relevant animal models of social stress and species that form strong adult social bonds have been utilized to study the etiology, treatment, and prevention of stress-related disorders. While undoubtedly a number of biological pathways contribute to the social buffering of the stress response, the convergence of evidence denotes the regulatory effects of oxytocin in facilitating social bond-promoting behaviors and their effect on the stress response. Thus, oxytocin may be perceived as a common regulatory element of the social environment, stress response, and stress-induced risks on mental and physical health.

The prevalence of allergic diseases has increased worldwide, a phenomenon that can be largely attributed to environmental effects. Among environmental factors, air pollution due to traffic is thought to be a major threat to childhood health. Residing near busy roadways is associated with increased asthma hospitalization, decreased lung function, and increased prevalence and severity of wheezing and allergic rhinitis. Recently, prospective cohort studies using more accurate measurements of individual exposure to air pollution have been conducted and have provided definitive evidence of the impact of air pollution on allergic diseases. Particulate matter and ground-level ozone are the most frequent air pollutants that cause harmful effects, and the mechanisms underlying these effects may be related to oxidative stress. The reactive oxidative species produced in response to air pollutants can overwhelm the redox system and damage the cell wall, lipids, proteins, and DNA, leading to airway inflammation and hyper-reactivity. Pollutants may also cause harmful effects via epigenetic mechanisms, which control the expression of genes without changing the DNA sequence itself. These mechanisms are likely to be a target for the prevention of allergies. Further studies are necessary to identify children at risk and understand how these mechanisms regulate gene-environment interactions. This review provides an update of the current understanding on the impact of air pollution on allergic diseases in children and facilitates the integration of issues regarding air pollution and allergies into pediatric practices, with the goal of improving pediatric health.

The social environment plays a considerable role in determining major psychiatric disorders. Emerging evidence suggests that features of the social environment modify gene expression independently of the primary DNA sequence through epigenetic processes. Accordingly, dysfunction of epigenetic mechanisms offers a plausible mechanism by which an adverse social environment gets “into the mind” and results in poor mental health. The purpose of this review is to provide an overview of the studies suggesting that epigenetic changes introduced by the social environment then manifest as psychological consequences. Our goal is to build a platform to discuss the ways in which future epidemiologic studies may benefit from including epigenetic measures. We focus on schizophrenia, major depressive disorder, post-traumatic stress disorder, anorexia nervosa, and substance dependence as examples that highlight the ways in which social environmental exposures, mediated through epigenetic processes, affect mental health.

Sexual health is important for general as well as reproductive health. The effects of the environment on sexual health are complex, however, because of the psychosomatic nature of human sexuality. The effects of any specific environmental agent on sexual function will therefore be modified or amplified by psychosocial factors, and any assessment of the effects of the agent will need to take those factors into account. As a consequence, we have little direct evidence of the adverse effects of the environment on sexuality. This paper therefore considers a) the aspects of sexuality that may by susceptible to environmental effects and the likely mediating mechanisms. These are considered under three headings: psychophysiological, endocrine, and subjective/interpersonal; b) the types of relevant environmental factors, including toxic pollutants, self-administered toxins, diet, situational factors, adversity, stress, and social and cultural factors. As yet research has not controlled adequately for the various confounding factors. It is suggested that a first step is to investigate the effects of work stress (e.g., shift and night work) on sexual relationships, comparing the effects across contrasting cultural settings. Such research would then provide a basis for cross-cultural study of other environmental factors.

Environmental and occupational risk factors contribute to nearly 40% of the national burden of disease in India, with air pollution in the indoor and outdoor environment ranking amongst leading risk factors. It is now recognized that the health burden from air pollution exposures that primarily occur in the rural indoors, from pollutants released during the incomplete combustion of solid fuels in households, may rival or even exceed the burden attributable to urban outdoor exposures. Few environmental epidemiological efforts have been devoted to this setting, however. We provide an overview of important available information on exposures and health effects related to household solid fuel use in India, with a view to inform health research priorities for household air pollution and facilitate being able to address air pollution within an integrated rural–urban framework in the future.

Objective

To review the recent (1995–2009) literature on psychosocial risk and protective factors for coronary heart disease (CHD) among women, including negative emotions, stress, social relationships, and positive psychological factors.

Methods

Articles for the review were identified using PubMed and bibliographies of relevant articles. Eligible studies included at least 100 women and either focused on (a) exclusively female participants or (b) both men and women, conducting either gender-stratified analyses or examining interactions with gender. Sixty-seven published reports were identified that examined prospective associations with incident or recurrent CHD.

Results

In general, evidence suggests that depression, anxiety disorders, anger suppression, and stress associated with relationships or family responsibilities are associated with elevated CHD risk among women, that supportive social relationships and positive psychological factors may be associated with reduced risk, and that general anxiety, hostility, and work-related stress are less consistently associated with CHD among women relative to men.

Conclusions

A growing literature supports the significance of psychosocial factors for the development of CHD among women. Consideration of both traditional psychosocial factors (e.g., depression) and factors that may be especially important for women (e.g., stress associated with responsibilities at home or multiple roles) may improve identification of women at elevated risk as well as the development of effective psychological interventions for women with or at risk for CHD.

Melatonin is an environmentally friendly-molecule with broad spectrum antioxidant capacity. Melatonin is widely present in the plant kingdom. High levels of melatonin exist in an aquatic plant, the water hyacinth, which is highly tolerant of environmental pollutants. Elevated levels of melatonin probably help plants to protect against environmental stress caused by water and soil pollutants. To investigate the potential relationships between melatonin supplementation and environmental tolerance in plants, pea plants were treated with high levels of copper in the soil. The results show that copper contamination kills pea plants; however, melatonin added to the soil significantly enhanced their tolerance to the copper contamination and, therefore, increased their survival. Based on the theory and these preliminary data, we speculate that melatonin could be used to improve the phytoremediative efficiency of plants against different pollutants. Since melatonin is safe to animals and humans as well as being inexpensive, it may be a feasible and cost-effective approach to clean environmental contaminations.

Rapidly expanding evidence increasingly strengthens the evidence linking psychological factors to asthma and allergy expression. Parallel studies in animals and humans demonstrating the influence of prenatal maternal stress and early caregiving experiences on the disrupted regulation of defensive biological systems [eg, sympathetic and adrenomedullary (SAM) system and the hypothalamicpituitary-adrenocortical (HPA) axis] provide strong proof of concept for this line of research. The consequent altered neuroimmune responses may influence the expression of immune-mediated disorders such as asthma as well as enhance an individual's susceptibility to other environmental factors that may also contribute to asthma risk.

Environmental risk assessment is an essential step in the development of solutions for pollution problems and new environmental regulations. An assessment system for environmental risks has been developed in China in recent decades. However, many of the Chinese technical guidelines, standards, and regulations were directly adapted from those of developed countries, and were not based on the Chinese environmental and socioeconomic context. Although existing environmental regulations for pollutants are usually obtained by extrapolations from high-dose toxicological data to low-dose scenarios using linear-non-threshold (LNT) models, toxicologists have argued that J-shaped or inverse J-shaped curves may dominate the dose–response relationships for environmental pollutants at low doses because low exposures stimulate biological protective mechanisms that are ineffective at higher doses. The costs of regulations based on LNT and J-shaped models could therefore be dramatically different. Since economic factors strongly affect the decision-making process, particularly for developing countries, it is time to strengthen basic research to provide more scientific support for Chinese environmental regulations. In this paper, we summarize current Chinese environmental policies and standards and the application of environmental risk assessment in China, and recommend a more scientific approach to the development of Chinese regulations.

Adults with mild intellectual disability (ID) experience stressful social interactions and often utilize maladaptive coping strategies to manage these interactions. We investigated the specific types of Active and Avoidant coping strategies reported by 114 adults with mild ID to deal with stressful social interactions. Open-ended responses to a sentence stem task were coded into five dimensions of Active and Avoidant coping. Adults with mild ID used Problem-Focused coping most frequently and this strategy was negatively correlated with psychological distress. Emotion-Focused coping was used infrequently but was also negatively related to psychological distress. Coping accounted for a significant portion of variance in psychological distress after controlling for perceptions of stressful social interactions. Findings have important implications for informing the development of interventions to enhance the ability of adults with mild ID to cope with stressful social interactions.

Background

James Tanner coined the expression `Growth as a Mirror' and summarized in four words the results of more than a century of research on growth. Nineteenth century social reformers saw poor child growth as a reflection of terrible environmental conditions of the working class. Later investigators in anthropology and other fields clarified the connections between poor nutrition, disease, psychosocial stress and poor growth.

Aim

To evaluate the growth as a mirror concept in light of recent studies of endocrine disruption.

Papers and Implications

Pollution is recognized as a prominent component of the modern environment. From studies of many pollutants it is clear that some pollutants depress growth while others speed sexual maturation and increase growth, primarily in weight and fatness. While such unwelcome environmental features do not always suppress growth, growth still mirrors the environment in all its complexity and this relationship is key to understanding growth patterns today. For example, Akwesasne Mohawk adolescents are characterized by high rates of obesity and overweight. Their growth reflects the multiple intersecting influences of psychosocial stress, several pollutant exposures and limited dietary chokes.

Conclusion

Although Tanner did not anticipate the myriad influences of pollutants, the growth as a mirror concept continues to have great validity and utility.

Abstinent alcoholics show a blunted stress cortisol response that may be a consequence of drinking or a preexisting risk marker. We tested cortisol responses to psychological stress in 186 18–30 year-old, healthy social drinkers having no personal history of alcohol or drug dependence, 91 of whom had one or two alcoholic parents (FH+) and 95 having no family alcoholism for two generations (FH−). We predicted that, similar to alcoholic patients, the FH+ would have reduced stress cortisol responses that would be partially determined by their temperament characteristics, specifically antisocial tendencies as measured by the California Psychological Inventory. On a stress day, subjects performed continuous simulated public speaking and mental arithmetic tasks for 45 min, and on a control day they sat and rested for the same time period. The FH+ who were low in sociability had smaller cortisol responses than FH−, high-sociability persons (t = 2.27, p = .O2). These two groups were not different in diurnal cortisol secretion patterns or affective responses to the stressors. Persons with a familial risk for alcoholism who have more antisocial tendencies may have altered central nervous system responses to emotionally relevant social challenges. Disrupted cortisol stress responses may serve as a risk marker for the development of substance use disorders.

Background

Little is known about environmental causes and contributing factors for autism. Basic science and epidemiologic research suggest that oxidative stress and inflammation may play a role in disease development. Traffic-related air pollution, a common exposure with established effects on these pathways, contains substances found to have adverse prenatal effects.

Objectives

We examined the association between autism and proximity of residence to freeways and major roadways during pregnancy and near the time of delivery, as a surrogate for air pollution exposure.

Methods

Data were from 304 autism cases and 259 typically developing controls enrolled in the Childhood Autism Risks from Genetics and the Environment (CHARGE) study. The mother’s address recorded on the birth certificate and trimester-specific addresses derived from a residential history obtained by questionnaire were geocoded, and measures of distance to freeways and major roads were calculated using ArcGIS software. Logistic regression models compared residential proximity to freeways and major roads for autism cases and typically developing controls.

Results

Adjusting for sociodemographic factors and maternal smoking, maternal residence at the time of delivery was more likely be near a freeway (≤ 309 m) for cases than for controls [odds ratio (OR) = 1.86; 95% confidence interval (CI), 1.04–3.45]. Autism was also associated with residential proximity to a freeway during the third trimester (OR = 2.22; CI, 1.16–4.42). After adjustment for socioeconomic and sociodemographic characteristics, these associations were unchanged. Living near other major roads at birth was not associated with autism.

Conclusions

Living near a freeway was associated with autism. Examination of associations with measured air pollutants is needed.