Abstracts: ISEE 20th Annual Conference, Pasadena, California, October 12–16, 2008: Contributed Abstracts
Laboratory studies in humans and animals have shown that air pollutants can enhance allergic inflammation and induce allergic immune responses. People with asthma have higher rates of sensitization and allergy and are more responsive to air pollutants’ effects on respiratory health; this is especially true in children. While it has been shown that exposure to traffic-related pollutants negatively impacts respiratory health, studies of the effect on allergen sensitization have not been consistent, perhaps due to differences in the populations studied with respect to age distributions, asthma status, and exposure assessment. The influence of traffic-related air pollutants during the prenatal period has not been investigated, although there is good reason to suspect a role, given the association between traffic-related pollutants and immune modulation.
An exploratory analysis was conducted to evaluate the association between prenatal and early-life exposures to outdoor air pollutants with allergic sensitization within a cohort of 232 children ages 6–11 years with asthma.
The data were obtained as part of the Fresno Asthmatic Children's Environment Study (n = 315) in the Central Valley of California. Only children for whom prenatal air pollution data could be obtained were included (n = 232). Prenatal and early-life exposure to ozone (O3), nitrogen dioxide (NO2), carbon monoxide (CO) and particulate matter with a median aerodynamic diameter ≤10 μm (PM10) was reconstructed for each child. Allergic sensitization was ascertained by skin-prick tests to 14 allergens. Predictive models were developed for sensitization to a) any allergen, b) at least one outdoor allergen, and c) at least one indoor allergen.
Nearly all (90%) of the children were born in California and 76% were born in the Fresno area. In multivariable analyses, higher exposure to CO and NO2 in the 2nd trimester was associated with increased sensitization to at least one outdoor allergen. The odds ratio was 1.54 (95% CI: 0.97, 2.45) per interquartile range (IQR) increase of NO2 during the 2nd trimester and OR = 1.61 (95%CI: 0.99, 2.70) for an IQR increase of CO during the 2nd trimester. No significant associations with the prenatal or early-life pollutant metrics considered were seen for sensitization to allergens in general or to at least one indoor allergen.
In this exploratory analysis of children with asthma, exposure to traffic-related pollutants during the 2nd trimester was associated with increased sensitization to outdoor allergens. The prenatal findings suggest the timing of the exposure may be more important than the overall dose and prenatal exposures are not just markers for lifetime or current exposures. This analysis lacked sufficient power to detect possible effect modification by factors such as parental allergen sensitization status, season of birth, gender, or housing characteristics such as gas stoves. Studies among more geographically diverse populations with larger exposure gradients may identify additional effects. Future prospective studies in larger populations are warranted to assess the timing of sensitization and identify possible susceptible subgroups. Studies within non-asthmatic cohorts are warranted.