Parental Stress Increases the Detrimental Effect of Traffic Exposure on Children's Lung Function (original) (raw)

Parental stress increases the effect of traffic-related air pollution on childhood asthma incidence

Proceedings of the National Academy of Sciences, 2009

Exposure to traffic-related pollution (TRP) and tobacco smoke have been associated with new onset asthma in children. Psychosocial stress-related susceptibility has been proposed to explain social disparities in asthma. We investigated whether low socioeconomic status (SES) or high parental stress modified the effect of TRP and in utero tobacco smoke exposure on new onset asthma. We identified 2,497 children aged 5-9 years with no history of asthma or wheeze at study entry (2002)(2003) into the Children's Health Study, a prospective cohort study in southern California. The primary outcome was parental report of doctor-diagnosed new onset asthma during 3 years of follow-up. Residential exposure to TRP was assessed using a line source dispersion model. Information about maternal smoking during pregnancy, parental education (a proxy for SES), and parental stress were collected in the study baseline questionnaire. The risk of asthma attributable to TRP was significantly higher for subjects with high parental stress (HR 1.51 across the interquartile range for TRP; 95% CI 1.16 -1.96) than for subjects with low parental stress (HR 1.05, 95% CI 0.74 -1.49; interaction P value 0.05). Stress also was associated with larger effects of in utero tobacco smoke. A similar pattern of increased risk of asthma was observed among children from low SES families who also were exposed to either TRP or in utero tobacco smoke. These results suggest that children from stressful households are more susceptible to the effects of TRP and in utero tobacco smoke on the development of asthma.

A Framework for Examining Social Stress and Susceptibility to Air Pollution in Respiratory Health

Environmental Health Perspectives, 2009

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 recom mend 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.

Air Pollution Exposure and Lung Function in Children: The ESCAPE Project

Environmental Health Perspectives, 2013

Background: There is evidence for adverse effects of outdoor air pollution on lung function of children. Quantitative summaries of the effects of air pollution on lung function, however, are lacking due to large differences among studies. oBjectives: We aimed to study the association between residential exposure to air pollution and lung function in five European birth cohorts with a standardized exposure assessment following a common protocol.

Relationship between air pollution, lung function and asthma in adolescents

Thorax, 2007

The interrelationships between air pollution, lung function and the incidence of childhood asthma have yet to be established. A study was undertaken to determine whether lung function is associated with new onset asthma and whether this relationship varies by exposure to ambient air pollutants. A cohort of children aged 9-10 years without asthma or wheeze at study entry were identified from the Children's Health Study and followed for 8 years. The participants resided in 12 communities with a wide range of ambient air pollutants that were measured continuously. Spirometric testing was performed and a medical diagnosis of asthma was ascertained annually. Proportional hazard regression models were fitted to investigate the relationship between lung function at study entry and the subsequent development of asthma and to determine whether air pollutants modify these associations. The level of airway flow was associated with new onset asthma. Over the 10th-90th percentile range of fo...

Personal and Ambient Air Pollution Exposures and Lung Function Decrements in Children with Asthma

Environmental Health Perspectives, 2007

BACKGROUND: Epidemiologic studies have shown associations between asthma outcomes and outdoor air pollutants such as nitrogen dioxide and particulate matter mass < 2.5 µm in diameter (PM 2.5). Independent effects of specific pollutants have been difficult to detect because most studies have relied on highly correlated central-site measurements. OBJECTIVES: This study was designed to evaluate the relationship of daily changes in percentpredicted forced expiratory volume in 1 sec (FEV 1) with personal and ambient air pollutant exposures. METHODS: For 10 days each, we followed 53 subjects with asthma who were 9-18 years of age and living in the Los Angeles, California, air basin. Subjects self-administered home spirometry in the morning, afternoon, and evening. We measured personal hourly PM 2.5 mass, 24-hr PM 2.5 elemental and organic carbon (EC-OC), and 24-hr NO 2 , and the same 24-hr average outdoor central-site (ambient) exposures. We analyzed data with transitional mixed models controlling for personal temperature and humidity, and as-needed β 2-agonist inhaler use. RESULTS: FEV 1 decrements were significantly associated with increasing hourly peak and daily average personal PM 2.5 , but not ambient PM 2.5. Personal NO 2 was also inversely associated with FEV 1. Ambient NO 2 was more weakly associated. We found stronger associations among 37 subjects not taking controller bronchodilators as follows: Personal EC-OC was inversely associated with morning FEV 1 ; for an interquartile increase of 71 µg/m 3 1-hr maximum personal PM 2.5 , overall percentpredicted FEV 1 decreased by 1.32% [95% confidence interval (CI),-2.00 to-0.65%]; and for an interquartile increase of 16.8 ppb 2-day average personal NO 2 , overall percent-predicted FEV 1 decreased by 2.45% (95% CI,-3.57 to-1.33%). Associations of both personal PM 2.5 and NO 2 with FEV 1 remained when co-regressed, and both confounded ambient NO 2. CONCLUSIONS: Independent pollutant associations with lung function might be missed using ambient data alone. Different sets of causal components are suggested by independence of FEV 1 associations with personal PM 2.5 mass from associations with personal NO 2 .

Prenatal particulate matter exposure and wheeze in Mexican children: effect modification by prenatal psychosocial stress

Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology, 2017

Air pollution exposure in childhood is associated with greater incidence and exacerbation of asthma, particularly in children whose parents report high levels of psychological stress. However, this interaction has not been completely elucidated in pregnancy. To examine whether the association between prenatal exposure to particulate matter no larger than 2.5 μm in diameter (PM2.5) and wheeze in children is modified by prenatal stress. Mexican women were recruited during pregnancy (N = 552). Residential prenatal daily exposure to PM2.5 was estimated using a satellite-based spatiotemporally resolved prediction model and averaged over trimesters. Maternal stress was indexed by maternal negative life events (NLE) score (range 0-11) ascertained during mid to late pregnancy. NLE scores were dichotomized at the median as low (NLE score ≤ 3) and high (NLE score > 3) stress. Reports of ever wheeze and wheeze in the past 12 months (current wheeze) for children were obtained using the Inter...

Chronic effects of air pollution on respiratory health in Southern California children: findings from the Southern California Children's Health Study

Journal of thoracic disease, 2015

Outdoor air pollution is one of the leading contributors to adverse respiratory health outcomes in urban areas around the world. Children are highly sensitive to the adverse effects of air pollution due to their rapidly growing lungs, incomplete immune and metabolic functions, patterns of ventilation and high levels of outdoor activity. The Children's Health Study (CHS) is a continuing series of longitudinal studies that first began in 1993 and has focused on demonstrating the chronic impacts of air pollution on respiratory illnesses from early childhood through adolescence. A large body of evidence from the CHS has documented that exposures to both regional ambient air and traffic-related pollutants are associated with increased asthma prevalence, new-onset asthma, risk of bronchitis and wheezing, deficits of lung function growth, and airway inflammation. These associations may be modulated by key genes involved in oxidative-nitrosative stress pathways via gene-environment inte...