Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2011 Jun;105(6):869-76.
doi: 10.1016/j.rmed.2010.11.022. Epub 2010 Dec 15.

Prenatal exposure to polycyclic aromatic hydrocarbons, environmental tobacco smoke and asthma

Maria José Rosa  1 , Kyung Hwa Jung, Matthew S Perzanowski, Elizabeth A Kelvin, Katherine W Darling, David E Camann, Steven N Chillrud, Robin M Whyatt, Patrick L Kinney, Frederica P Perera, Rachel L Miller
Affiliations

Prenatal exposure to polycyclic aromatic hydrocarbons, environmental tobacco smoke and asthma

Maria José Rosa et al. Respir Med. 2011 Jun.

Abstract

Background: Previously, we reported that prenatal exposures to polycyclic aromatic hydrocarbons (PAH) and postnatal environmental tobacco smoke (ETS) in combination were associated with respiratory symptoms at ages 1 and 2 years. Here, we hypothesized that children exposed to both prenatal PAH and ETS may be at greater risk of asthma and seroatopy at ages 5-6 years, after controlling for current pollution exposure.

Methods: Prenatal PAH exposure was measured by personal air monitoring over 48 h. ETS exposure, respiratory symptoms and asthma at ages 5-6 years were assessed through questionnaire. Immunoglobulin (Ig) E was measured by Immunocap.

Results: A significant interaction between prenatal PAH and prenatal (but not postnatal) ETS exposure on asthma (p < 0.05), but not IgE, was detected. Among children exposed to prenatal ETS, a positive nonsignificant association was found between prenatal PAH exposure and asthma (OR 1.96, 95% CI [0.95-4.05]). Among children without exposure to prenatal ETS, a negative nonsignificant association was found between prenatal PAH exposure and asthma (OR 0.65, 95% CI [0.41-1.01]). Prenatal PAH exposure was not associated with asthma or IgE at age 5-6 years.

Conclusions: Combined prenatal exposure to PAH and ETS appears to be associated with asthma but not seroatopy at age 5-6. Exposure to PAH alone does not appear associated with either asthma or seroatopy at age 5-6 years. Discerning the differential effects between ETS exposed and ETS nonexposed children requires further study.

PubMed Disclaimer

References

    1. Jaakkol JJK, Vutanen M, Heinonen P. Low-Level Air Pollution. American Journal of Public Health. 1991;81:6–9. - PMC - PubMed
    1. Kagawa J. Atmospheric pollution due to mobile sources and effects on human health in Japan. Environmental health perspectives. 1994;102(Suppl):93–9. - PMC - PubMed
    1. Samet JM, Dominici F, Curriero FC, Coursac I, Zeger SL. Fine particulate air pollution and mortality in 20 U.S. cities, 1987–1994. N Engl J Med. 2000;343(24):1742–9. - PubMed
    1. Morgenstern V, Zutavern A, Cyrys J, Brockow I, Koletzko S, Kramer U, et al. Atopic diseases, allergic sensitization, and exposure to traffic-related air pollution in children. Am J Respir Crit Care Med. 2008;177(12):1331–7. - PubMed
    1. Riedl M, Diaz-Sanchez D. Biology of diesel exhaust effects on respiratory function. J Allergy Clin Immunol. 2005;115(2):221–8. quiz 9. - PubMed

Publication types

Substances