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 . It is possible that associations between allergic respiratory illnesses and traffic density are due to NAAQS criteria air pollutants, particularly NO2, which is directly related to local traffic density . Krämer et al. assessed this possibility in a study of 306 children 9 years of age living at least 2 years in a home near major roads in Germany . Using passive samples with Palmes tubes, weekly average concentrations were measured for personal NO2 in March and September, and for outdoor home or near home NO2 at 158 locations in each of four seasons . Investigators showed that outdoor NO2 was a good predictor of home traffic density but a poor predictor for personal NO2 exposure reflecting the known importance of indoor NO2 sources. They followed the children with weekly parental questionnaires for atopic symptoms for 1 year. In suburban areas there was little variation in outdoor NO2, and inclusion of suburban subjects in regression models decreased parameter estimates and increased standard errors. For urban areas , they found that atopic sensitizations to pollen, to house dust mite or cat, and to milk or egg were each significantly associated with outdoor NO2 but not predicted personal NO2. They also found that outdoor NO2, but not predicted personal NO2, was significantly associated with reports of at least 1 week with symptoms of wheezing and of allergic rhinitis. Relationships for atopy and rhinitis symptoms by quartile of outdoor NO2 suggested a dose–response relationship . Although an ever diagnosis of hay fever was associated with outdoor NO2, diagnosed asthma was not . The maximum outdoor NO2 of the urban sites was 36 ppb ,vertical grow system which is far less than the U.S. EPA NAAQS of 53 ppb annual mean . The overall results suggest that outdoor NO2 was serving as a marker for more causal airborne agents rather than a direct effect of NO2.

High personal exposures to PAHs near busy streets were possible in the study by Krämer et al. , as well as other studies in Table 2 for high traffic density. Dubowsky et al. measured total real-time, particle bound PAHs from three nonsmoking indoor sites with different traffic densities characteristic of urban, semiurban, and suburban residencies.A significant contribution of traffic related PAHs to indoor PAHs was detected. Indoor peaks occurred during morning rush hour on weekdays only . The geometric means of PAHs corrected for indoor sources were urban, 31 ng/m3; semiurban, 19 ng/m3; and suburban, 8 ng/m3. Despite the suggestion that NO2 may be acting as a surrogate pollutant, the respiratory effects of NO2 are still important. However, the magnitudes of effects of NO2 on asthma are not entirely clear, and there are considerable inconsistencies in the experimental literature. Some studies have shown alterations in lung function, airway responsiveness, or symptoms, whereas others have not, even at high concentrations [reviewed by Bascom et al. ]. Data that support the traffic density studies come from a clinical crossover study that used ambient exposures of 20 mild pollen-allergic adult asthmatic individuals . Subjects showed early- and late-phase bronchospastic reactions to pollen allergen challenge that were greater 4 hr after a 30-min exposure in a car parked in a road tunnel compared with a low control exposure in a suburban hotel . Specific airway resistance 15 min after allergen challenge increased 44% in 12 subjects exposed to road tunnel NO2 > 159 ppb compared with 24% for their control exposures . The higher NO2 tunnel exposures were associated with significantly more symptoms and beta-agonist inhaler use 18 hr after allergen challenge. In addition, FEV1 decreased significantly more than with control exposures 3–10 hr after allergen challenge . Effects were smaller using PM10 or PM2.5 as the exposure metric. The authors compared their results with those from earlier chamber studies using 265 ppb NO2 before allergen challenge.

They concluded that although those results also showed an enhancement of early- and late-phase asthmatic reactions , effects were greater for lower NO2 exposures in the tunnel, suggesting other pollutants were important. Other agents aside from either NAAQS criteria air pollutants or air toxics could explain some part of the association of asthma and allergy outcomes with traffic density. Latex allergen found on respirable rubber tire particles is likely common in urban air and could lead to sensitization and respiratory symptoms. In addition, the physical action of motor vehicles on road dust, which is known to contain pollen grains, could lead to the production and resuspension of smaller respirable pollen fragments . Other allergenic bioaerosols such as fungal spores could be fragmented and resuspended as well. Interactions between pollutants and allergens could also influence effects. Allergenic molecules could be delivered to target sites in the airways on diesel carbon particles. as evidenced in vitro using the rye grass pollen allergen Lol p1 . Another study using immunogold labeling techniques found that indoor home soot particles, primarily in the sub-micrometer size range, had bound antigens of cat , dog , and birch pollen , and this adsorption was replicated in vitro with DEP particles . Other biologic interactions between pollutants and allergens on airways that favor inflammatory reactions have been hypothesized , including enhancement of allergen sensitization in asthmatic children with ETS exposure and pollutant-induced enhancements of the antigenicity of allergens .Experimental evidence supports the biologic plausibility of a role for PAHs from fossil fuel combustion products in the onset and exacerbation of asthma. However, the occupational data on DE and asthma onset are limited to one three-case series. In addition, despite high exposures, overall inconsistency is found in occupational studies of respiratory symptoms or lung function and diesel/gas exhaust exposures. Bias from the healthy worker effect is likely given the expectation of avoidance behavior among individuals with respiratory sensitivity to inhaled irritants, including asthmatics. This behavior has been hypothesized to result from a toxicant-induced loss of tolerance . The inconsistent and weak occupational evidence does not rule out different dose–response relationships for asthma in nonoccupational settings. Epidemiologic results showing associations between childhood asthma and ETS may be explained, in part, by PAHs. Positive results in epidemiologic studies of asthma and traffic-related exposures also may be explained, in part, by PAHs.

The question that remains is, what are the determinants of asthma associations with complex mixtures of ETS-related and traffic-related particle components and gases? The above review gives the overall impression that asthma,indoor weed growing accessories related respiratory symptoms, lung function deficits, and atopy are higher among people living near busy traffic. Some data coherent with this view are found in studies showing a higher prevalence of asthma and atopic conditions in more developed Westernized countries and in urban compared with rural areas [reviewed by Beasley et al. and Weinberg ]. For instance, studies in Africa have shown that pediatric asthma is rare in rural regions, whereas African children living in urban areas have experienced an increasing incidence of asthma . The urban-rural differences have tended to narrow as rural Africans became more Westernized . This suggests that the increase of asthma seen in developed countries may be attributable to some component of urbanization, including automobile and truck traffic. However, this urbanization gradient is not a consistent finding across the literature . For instance, in the traffic exposure–response study by Montnémery et al. , although there were significant associations of asthma symptoms and diagnosis to traffic density, there were no urban-rural differences. In addition, some recent studies that specifically examined farming environments, found a decreased risk of asthma and atopy among children living on farms , particularly where there is regular contact with farm animals. This prompted these investigators to hypothesize that a “protective farm factor” may reflect the influence of microbial agents on TH1 versus TH2 cell development or reflect the development of immuno tolerance . This possibility, in addition to potentially high levels of confounding by uncontrolled factors that vary by geography, makes it difficult to clearly interpret the cross-sectional studies on urban versus rural areas or ecologic studies of international differences.The following section will examine the epidemiologic literature on the relationship of asthma and atopy in children to formaldehyde. This serves to exemplify one of the few low molecular weight agents associated with asthma in both the occupational and nonoccupational literature, and to exemplify an air toxic that has effects from low to high exposure levels. However, there are little available nonoccupational data on the risk of asthma onset from formaldehyde. One study passively measured formaldehyde over 2 weeks in the homes of 298 children and 613 adults . In log-linear models controlling for SES variables and ethnicity, the study found a significantly higher prevalence of physician-diagnosed asthma and chronic bronchitis in children 6–15 years of age living in homes with higher formaldehyde concentrations over 41 ppb . However, the room specific measurements revealed that the association was attributable to high formaldehyde concentrations in kitchens, particularly those homes with ETS exposures , suggesting possible confounding by other factors not measured. In random effects models controlling for SES and ETS, they found significant inverse associations between morning PEF rates and average formaldehyde from the bedroom, and between evening PEF and household average formaldehyde.

There was no apparent threshold level. The PEF finding was independent of ETS, but the effects of age or of anthropomorphic factors were not mentioned. Symptoms of chronic cough and wheeze were higher, and PEF lower, in adults living in houses with higher formaldehyde levels. There was a significant interaction between formaldehyde and tobacco smoking in relation to cough in adults. Passive measurements of NO2 did not confound the associations in children or adults. Other nonoccupational data on formaldehyde relate indirectly to asthma. Wantke et al. evaluated levels of specific IgE to formaldehyde using RAST in 62 eight-year old children attending one school with particleboard paneling and urea foam window framing. The children were transferred to a brick building because of elevated formaldehyde levels in particleboard classrooms and complaints of headache, cough, rhinitis, and nosebleeds. Symptoms and specific IgE were examined before and 3 months after cessation of exposure. At baseline, three children had RAST classes ≥ 2 and 21 had classes ≥ 1.3 , whereas all 19 control children attending another school had classes < 1.3. After transfer, the RAST classes significantly decreased from 1.7 ± 0.5 to 1.2 ± 0.2 , and symptoms decreased. However, IgE levels did not correlate with symptoms. None of the children had asthma. Garrett et al. hypothesized that formaldehyde may adversely affect the lower respiratory tract by increasing the risk of allergic sensitization to common allergens. They studied 43 homes with at least one asthmatic child and 37 homes with only nonasthmatic children . Atopy was evaluated in the children with SPTs for allergy to 12 common animal, fungal, and pollen allergens. Formaldehyde was measured passively throughout the homes over 4 days in four different times of 1 year. Atopic sensitization by SPT was associated with formaldehyde levels [OR for 20 µg/m3 increase, 1.42 ]. Across three formaldehyde exposure categories, there was also a significant increase in the number of positive SPTs and in the wheal ratio of allergen SPT over histamine SPT. Mean respiratory symptom scores were significantly and positively associated across the three categories. There was a significant positive association between parent-reported, physician-diagnosed asthma and formaldehyde, but this was confounded by history of parental asthma and parental allergy. It is unclear why these familial determinants were treated as confounders rather than effect modifiers, although knowledge of asthma by parents may lead to bias in the assessment of asthma in their children. Several other studies of nonasthmatic subjects have examined health outcomes and biomarkers that are relevant to asthma. Franklin et al. studied 224 children 6–13 years of age with no history of upper or lower respiratory tract diseases, using expired nitric oxide as a marker for lower airway inflammation . Formaldehyde was passively monitored in the children’s homes for 3–4 days.