Case-control study of hospital admission with asthma in children aged 5-14 years: relation with road traffic in north west London

Wilkinson, Paul; Elliott, Paul; Grundy, Chris; Shaddick, Gavin; Thakrar, Bharat; Walls, P; Falconer, Sharon

doi:10.1136/thx.54.12.1070

Cited by 91 publications

(63 citation statements)

References 15 publications

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“…Recent studies in California evaluating childhood cancer and traffic density have generally found no association (Reynolds et al, 2001;Langholz et al, 2002;Reynolds et al, 2002). Some studies have found an association between traffic volume and the number of hospital admissions for asthma (English et al, 1999), vehicle or truck traffic and self-reported symptoms of asthma (Weiland et al, 1994;Duhme et al, 1996), but others have found no association between asthma and traffic volume (Wilkinson et al, 1999). Truck and road traffic were related to chronic respiratory symptoms and reduced lung function in studies of adolescents (Wjst et al, 1993;Oosterlee et al, 1996;Van Vliet et al, 1997;Brunekreef et al, 1997;Ciccone et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Traffic density in California: Socioeconomic and ethnic differences among potentially exposed children

Gunier

Hertz

Behren

et al. 2003

J Expo Sci Environ Epidemiol

188

135

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Motor vehicles are the main source of many hazardous air pollutants in California. Previous studies have shown that low-income and minority populations are more likely to live near industrial sources of pollution and in areas that do not meet national air quality standards. We estimated neighborhood exposures to motor vehicle emissions from a road network with daily traffic counts using a geographic information system. To calculate traffic density, we summed the average daily vehicle miles of travel per square mile of land area for each census block group in the state. We used 1990 census data to characterize the population by age, race and socioeconomic status in block groups with high traffic density. Block groups with more than 500,000 vehicle miles of travel per square mile were defined to be high traffic density. Statewide, about 5% of all block groups met this criterion and more than 215,000 children under 15 years of age lived in these high traffic density areas. Block groups in the lowest quartile of median family income were three times more likely to have high traffic density than block groups in the highest income quartile. The percentage of children living in high traffic density block groups increased with decreasing median family income for all race and ethnicities except White. Overall, children of color were about three times more likely to live in high-traffic areas than were white children. Based on this analysis, low-income and children of color have higher potential exposure to vehicle emissions. Future exposure assessment studies should target the highest traffic density areas, and health studies should consider the differences by income and race or ethnicity during design.

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Section: Introductionmentioning

confidence: 99%

Traffic density in California: Socioeconomic and ethnic differences among potentially exposed children

Gunier

Hertz

Behren

et al. 2003

J Expo Sci Environ Epidemiol

188

135

View full text Add to dashboard Cite

show abstract

“…All but one were conducted in Europe and Asia ( Table 2). Fifteen of these have been in children (96)(97)(98)(99)(100)(101)(102)(103)(104)(105)(106)(107)(108)(109)(110), four in adults (111)(112)(113)(114), and one study in both children and adults (115).…”

Section: Epidemiologic Evidence For Pollutant Mixtures Containing Pahmentioning

confidence: 99%

“…Krämer et al (109) conducted a cross-sectional study of atopic sensitization and asthma diagnosis but had a prospective outcome assessment of atopic symptoms for 1 year along with seasonal NO 2 measurements. Other designs include three case-control studies of hospital admissions (97,99,108), and one case-control study of California Medicaid claims for asthma (105). Another study was a mixture of cross-sectional, surveynested case-control, and historical cohort (110).…”

Section: Epidemiologic Evidence For Pollutant Mixtures Containing Pahmentioning

confidence: 99%

Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.

Delfino

2002

Environ Health Perspect

268

152

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Outdoor ambient air pollutant exposures in communities are relevant to the acute exacerbation and possibly the onset of asthma. However, the complexity of pollutant mixtures and etiologic heterogeneity of asthma has made it difficult to identify causal components in those mixtures. Occupational exposures associated with asthma may yield clues to causal components in ambient air pollution because such exposures are often identifiable as single-chemical agents (e.g., metal compounds). However, translating occupational to community exposure-response relationships is limited. Of the air toxics found to cause occupational asthma, only formaldehyde has been frequently investigated in epidemiologic studies of allergic respiratory responses to indoor air, where general consistency can be shown despite lower ambient exposures. The specific volatile organic compounds (VOCs) identified in association with occupational asthma are generally not the same as those in studies showing respiratory effects of VOC mixtures on nonoccupational adult and pediatric asthma. In addition, experimental evidence indicates that airborne polycyclic aromatic hydrocarbon (PAH) exposures linked to diesel exhaust particles (DEPs) have proinflammatory effects on airways, but there is insufficient supporting evidence from the occupational literature of effects of DEPs on asthma or lung function. In contrast, nonoccupational epidemiologic studies have frequently shown associations between allergic responses or asthma with exposures to ambient air pollutant mixtures with PAH components, including black smoke, high home or school traffic density (particularly truck traffic), and environmental tobacco smoke. Other particle-phase and gaseous co-pollutants are likely causal in these associations as well. Epidemiologic research on the relationship of both asthma onset and exacerbation to air pollution is needed to disentangle effects of air toxics from monitored criteria air pollutants such as particle mass. Community studies should focus on air toxics expected to have adverse respiratory effects based on biological mechanisms, particularly irritant and immunological pathways to asthma onset and exacerbation.

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“…Nuisances perception at home was also suggested as a good proxy for traffic -related air pollution in Switzerland (Oglesby et al, 2000 ). Following the same rationale as the VESTA ''traffic density'' index, some studies combined traffic and distance data (Wilkinson et al, 1999;Pearson et al, 2000). In a recent case -control study of air pollution from traffic and childhood cancer, two cumulated exposure indices were also accommodated, as in the present study, with the same Danish OSPM software that is built in the ExTra model (Raaschou -Nielson et al, 2000;RaaschouNielson et al, 2001 ).…”

Section: Discussionmentioning

confidence: 99%

Five Epidemiological Studies on Transport and Asthma: Objectives, design and descriptive results

Zmirou¹,

Gauvin²,

et al. 2002

J Expo Sci Environ Epidemiol

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A case -control study was conducted in five French metropolitan areas in order to assess the role of traffic -related air pollution in the occurrence of childhood asthma. This paper presents the study design and describes the distribution of key exposure variables. A set of 217 pairs of matched 4 -to 14 -year -old cases and controls were investigated ( matching criteria: city, age, and gender ). Current and past environmental smoke exposures, indoor allergens or air pollution sources, and personal and family atopy were assessed by standard questionnaires. When possible, direct measurements were done to check the validity of this information, on current data: skin prick tests, urine cotinine, house dust mites densities, personal exposures to, and home indoor concentrations of NO x and PM 2.5 . Cumulative exposure to traffic -related pollutants was estimated through two indices: ''traffic density'' refers to a time -weighted average of the traffic density -to -road distance ratio for all home and school addresses of each child's life; ''air pollution'' index combines lifelong time -activity patterns and ambient air concentration estimates of NO x , using an air dispersion model of traffic exhausts. Average current PM 2.5 personal exposure is 23.8 g / m 3 ( SD = 17.4 ), and average indoor concentrations = 22.5 g / m 3 ( 18.2 ); corresponding values for NO 2 are 31.4 ( 13.9 ) and 36.1 ( 21.4 ) g / m 3 . Average lifelong calculated exposures to traffic -related NO x emissions are 62.6 g / m 3 ( 43.1 ). The five cities show important contrasts of exposure to traffic pollutants. These data will allow comparison of lifelong exposures to indicators of traffic exhausts between cases and controls, including during early ages, while controlling for a host of known enhancers or precipitators of airway chronic inflammation and for possible confounders.

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Case-control study of hospital admission with asthma in children aged 5-14 years: relation with road traffic in north west London

Cited by 91 publications

References 15 publications

Traffic density in California: Socioeconomic and ethnic differences among potentially exposed children

Traffic density in California: Socioeconomic and ethnic differences among potentially exposed children

Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.

Five Epidemiological Studies on Transport and Asthma: Objectives, design and descriptive results

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