Evidence for a healthy worker effect is that in many of the studies, workers had higher baseline FEV1 values compared with those of control groups or with advancing tenure . There is other evidence in the occupational literature on diagnosed occupational asthma in bakers, and on allergic sensitization to platinum salts and to TDI, that risk is greatest in the initial 1- to 2-year period of employment . Except for the case report of “diesel asthma” , none of the occupational studies reviewed above performed standard spirometric tests to diagnose asthma, and none followed workers prospectively from the start of employment.One common indoor air pollutant high in PAHs is environmental tobacco smoke . ETS also contains other toxic air pollutants, including 29 air toxics of 49 major components , making it difficult to ascribe effects to any one pollutant.This suggests an acute enhancement of IgE responses is possible, but whether the initial expression of allergic sensitization is enhanced by ETS is in dispute. A quantitative meta-analysis of studies up to April 1997 showed no association between parental smoking during pregnancy or infancy and atopic sensitization by skin prick tests in children without asthma or wheezing disorders . There was considerable inconsistency across studies . Other more-recent reviews have concluded that the relationship between ETS exposurein school-age children and the development of both asthma and allergy is poorly understood . A recent study of 5,762 school-age children had sufficient power to find a significant association between in utero exposure to maternal smoking without subsequent ETS exposure and history of physician diagnosed asthma, current asthma, and asthma requiring medication .
The same study showed that although current or past ETS exposure occurring only after birth was associated with reports of wheezing,grow racking it was not associated with asthma prevalence. Furthermore, combined in utero plus postnatal exposures did not increase risk of asthma beyond in utero exposures alone. The finding that maternal smoking during pregnancy has a stronger relationship to asthma onset than later ETS exposures was supported by several other studies that separated maternal in utero exposures from postnatal exposures . It is conceivable that in utero exposures to ETS shifts the immune response toward a TH2-type pattern as a result of the adjuvant action of PAH components interacting with in utero allergen exposures, which are now believed to lead to atopic sensitization before birth . It is plausible that postnatal coexposures would do the same, but the epidemiologic data are inconsistent for the relationship between ETS exposure and childhood asthma incidence. On the other hand, there is a preponderance of evidence linking ETS to acute exacerbations of asthma in asthmatic children. A recent meta-analysis concluded that studies showed an excess incidence of wheezing in smoking households, particularly in nonatopic children, suggesting a “wheezy bronchitis” pattern; however, in children with diagnosed asthma, parental smoking was associated with greater severity rather than incidence . A quantitative meta-analysis of studies up to April 1997 for 25 studies of asthma prevalence showed a pooled odds ratio for asthma of 1.21 if either parent smoked . Well-conducted panel studies are still needed to evaluate acute exposure–response relationships using repeated measures methods. A recent daily panel study over 3 months in 74 asthmatic children showed that acute asthma symptom severity, PEF, and bronchodilator use was associated with ETS exposure . There is less information about adultonset asthma. A cohort study of 451 nonsmoking asthmatic adults found that acute asthma severity, asthma-specific quality of life, and health status were associated with self-reported ETS exposure . Cohort studies have also shown increased risk of developing adult asthma from ETS , including occupational exposures . Among 3,914 nonsmoking adults followed 10 years, the relative risk for asthma onset from 10 years of working with a smoker was 1.45 .
A large survey of 4,197 never-smoking adults showed an elevated risk of physician-diagnosed asthma from any ETS exposure [OR 1.39 ] but no increased risk of allergic rhinitis . Reviews that have included other epidemiologic studies have concluded that although ETS is consistently associated with adult asthma onset, the number of studies is limited and the magnitude of effects are small, with limited dose–response information . One question that remains to be answered is what are the chemical determinants of associations between asthma and ETS, which is a complex mixture of particle and gas-phase components? Do PAHs play a major role in these associations?The urban exposure most relevant to the potential importance of PAHs to asthma is exposure to automobile and truck traffic. An earlier descriptive study spurred interest in potential adjuvant effects of DEP on IgEmediated respiratory allergic responses . This was a cross-sectional study of 3,133 Japanese persons that showed the prevalence of cedar pollen allergy was higher near busy highways despite equivalent local exposure to cedar pollen in less-busy areas. No epidemiologic studies have used quantitative exposure estimates of either DEP or ambient PAHs. However, European research has had access to black smoke measurements. A panel study of 61 children in the summer showed stronger associations for black smoke than for PM10 in relation to PEF, respiratory symptoms, and bronchodilator use . The authors hypothesized that black smoke may be a better surrogate for fine particles emitted by diesel engines or for other chemicals that may be the causal components in DE. Ambient NO2 could additionally serve as a marker for traffic exposure. Studnicka et al. explicitly used outdoor NO2 as a surrogate to show “traffic-related pollution” was associated with asthma prevalence among 843 children living in areas of lower Austria without local industrial emissions of air pollution. Numerous epidemiologic studies have shown associations between traffic density and asthma prevalence or morbidity. All but one were conducted in Europe and Asia . Fifteen of these have been in children , four in adults , and one study in both children and adults . All but seven have been purely cross-sectional studies. Krämer et al. 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 NO2 measurements. Other designs include three case–control studies of hospital admissions , and one case–control study of California Medicaid claims for asthma .
Another study was a mixture of cross-sectional, survey nested case–control, and historical cohort . One study of adult Japanese women was cross-sectional for symptom prevalence and also tested longitudinal models for 10 seasonal repeated measures for lung function in a sub-sample . Eleven looked at traffic density, but no air pollution measurements were used in effect estimates or as confirmation of exposure gradients ; four had traffic density, black smoke and/or NO2 ; and five used combustion-related air pollution measurements near the home as modeled surrogates for traffic exposures . Hirsch et al. briefly mentioned results for truck traffic, focusing instead on predicted home exposures from one hundred eighty-two 1-km2 grid measurements of CO, benzene, NO2, SO2, and O3. Pershagen et al. used predicted NO2 from models involving traffic data near the home and background ambient NO2 data,grow racks indoor with home residence time as a weighting factor. Oosterlee et al. investigated respiratory symptom prevalence and asthma in relation to busy and quiet streets predicted with model calculations of NO2 concentrations using the Dutch CAR model . Only four studies have separately assessed exposures from truck versus automobile traffic , two of which examined the same children in South Holland using actual 1-year measurements of traffic density in relation to lung function and symptoms . Another study in Germany had only self-reported truck traffic density in relation to symptoms . Except for one study , all of the above studies examining truck traffic showed increased risks in respiratory symptoms including wheeze from higher truck traffic density near the home . The Holland studies showed greater increased risks in respiratory symptoms including wheeze and lung function deficits from higher truck traffic than from automobile density near the home. Both Holland studies confirmed the possible relevance of DE by finding that black smoke measurements at the children’s schools were also associated with increased symptoms and lung function deficits . Astudy in Italy also found increased prevalence of asthma and symptoms from truck and bus traffic but not overall traffic . Only the study by Wyler et al. failed to show any difference between truck and car traffic in strengths of association; positive associations were limited to atopic sensitization. Although most of the traffic studies did not report associations by gender, four did find adverse effects of traffic-related exposures in children to be stronger in girls than in boys , while two other showed null results for both genders . In the study by Wyler et al. in adults, associations between pollen sensitization and home traffic density were larger for women than men. These gender differences are unexplained. Although differences in the perception of symptoms or reporting bias are possible, this does not explain the considerably larger lung function deficits in girls reported by Brunekreef et al. .
Negative results in the studies of traffic related exposures may be due to weaknesses that lead to exposure and outcome misclassification, which generally, but not always, lead to bias toward the null hypothesis if the misclassification is independent of systematic errors . This bias was possible in studies that used are awide exposure estimates without assessments of micro-environmental exposures or traffic near the home and school , or that relied entirely or partly on self-reported exposures . Nevertheless, most of these studies still showed positive associations between traffic and respiratory outcomes. Except for pulmonary function tests and tests for atopic sensitization , respiratory outcomes, including physician-diagnosed illnesses, were either abstracted from administrative databases or self-reported for the remaining studies. All but a sub-sample of two studies were subject to cross sectional or case–control biases. One of these biases stems from the use of current exposure. Current exposure may not be a good surrogate for exposure during past times that are more temporally relevant to current disease status. This is because outcomes may have an onset in the past, or because outcomes were previous illnesses or exacerbations of disease recalled in survey questionnaires. An important assumption is that current residence near traffic is a proxy for past exposures, and some, but not all, of the studies screened for residence times . One resultant systematic bias that could lead to null results is differential migration away from busy streets by symptomatic subjects. This is supported by the finding of Oosterlee et al. that parents with children having respiratory symptoms live an average of 2.6 years shorter at the present address than those of asymptomatic children. A positive bias, on the other hand, could have occurred from socioeconomic status , which was not always controlled for. This is important because people living on busy streets may be poorer. Clearly, well-designed prospective cohort studies and repeated measures panel studies are needed to assess the question of whether exposure to primary pollutants from traffic, which include air toxics, are risk factors for the onset or exacerbation of asthma and other respiratory allergic illnesses in children and adults. One epidemiologic approach that may prove useful to define source-specific air pollutant exposures such as traffic-related exposures is the use of principal component factor analysis with varimax rotation using available criteria pollutant data. One large survey study used this approach in Taiwan . They recruited 331,686 middle school children who were nonsmokers and were enrolled in schools within 2 km of 1 of 55 monitoring stations. They compared asthma prevalence rates with air pollution concentrations and found positive associations with asthma prevalence for NOx and CO. These gases had factor loadings over 0.91, along with inverse loadings for O3 of –0.92, likely from scavenging of O3 by NOx . For an interquartile increase in CO and in NOx , the prevalence of either physician diagnosed or questionnaire-based asthma increased around 1% for both boys and girls. Asthma was not associated with PM10 or SO2, except for an unexpected inverse association in boys for PM10. The association of acute asthma with CO is supported in a Seattle panel study of 133 asthmatic children and is likely explained by more causal components of vehicle exhaust and other combustion byproducts .