Polycyclic Aromatic Hydrocarbons, Environmental Tobacco Smoke, and Respiratory Symptoms in an Inner-city Birth Cohort

Abstract

Study objectives-Several studies have found associations between diesel exposure, respiratory symptoms, and/or impaired pulmonary function. We hypothesized that prenatal exposure to airborne polycyclic aromatic hydrocarbons (PAH), important components of diesel exhaust and other combustion sources, may be associated with respiratory symptoms in young children. We also hypothesized that exposure to environmental tobacco smoke (ETS) may worsen symptoms beyond that observed to be associated with PAH alone.Design/participants-To test our hypotheses, we recruited 303 pregnant women from northern Manhattan believed to be at high risk for exposure to both PAH and ETS, collected 48-h personal PAH exposure measurements, and monitored their children prospectively.Results-By 12 months of age, more cough and wheeze were reported in children exposed to prenatal PAH in concert with ETS postnatally (PAH × ETS interaction odds ratios [ORs], 1.41 [p < 0.01] and 1.29 [p < 0.05], respectively). By 24 months, difficulty breathing and probable asthma were reported more frequently among children exposed to prenatal PAH and ETS postnatally (PAH × ETS ORs, 1.54 and 1.64, respectively [p < 0.05]).Conclusions-Our results suggest that early exposure to airborne PAH and ETS can lead to increased respiratory symptoms and probable asthma by age 12 to 24 months. Interventions to lower the risk of respiratory disease in young children living in the inner city may need to address the importance of multiple environmental exposures. Keywords asthma; environmental tobacco smoke; polycyclic aromatic hydrocarbons Living in high-traffic areas and/or exposure specifically to diesel exhaust particles (DEP) have been associated with increased respiratory symptoms and impaired lung function in children. 1-5 Because of these epidemiologic findings, the concerns over the health risk following exposure to DEP that comprise vehicle exhaust emissions have extended beyond cancer to added concerns of impaired pulmonary health and asthma. In addition, higher DEP exposure has been associated with a greater risk of becoming sensitized to pollen, 4 as well as polarization of the local cytokine environment toward the development of T-helper type 2 cytokine responses that are thought to underlie atopy or allergic asthma. 6,7The particulate fraction of DEP is formed mainly of elemental carbon particles to which organic compounds, including polycyclic aromatic hydrocarbons (PAH), are adsorbed. The relatively small size (ie, mass median diameter of 0.05 to 0.3 μm) of DEP facilitates their deep penetration in the respiratory system, 8 and multiple mechanisms have been proposed for their effects on airway inflammation. These include increased cytokine production, altered oxidative processes, up-regulated chemokine production (ie, regulated upon activation, normal T-cell expressed and secreted, and monocyte chemotactic protein-1), increased free-radical formation, increased nitric oxide, and direct binding of DEP to allergens. 9 PAH that usually comprise DEP specif...

Polycyclic Aromatic Hydrocarbons Impair Function of β2-Adrenergic Receptors in Airway Epithelial and Smooth Muscle Cells

“…In previous work from the CCCEH, pregnant Dominican and AfricanAmerican women, aged [18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35] (2,15). A PAH mixture that reproduced the PAH exposure of the CCCEH participants (Table 1) was produced for our cellular experiments.…”

“…In a second pathway, exposure to diesel may provide a strong adjuvant for allergic sensitization, and such exposure was shown to up-regulate allergic immune mechanisms in the airways (4,(30)(31)(32)(33). PAHs, which are components of exhaust from the incomplete combustion of diesel fuel, were linked directly with the development of respiratory disease by our group (2,7). Mechanistic experiments so far suggest that the inhalation of PAHs can cause acute airway inflammation via the induction of genes associated with the aryl hydrocarbon receptor, oxidative stress, and inflammation (34).…”

“…All of these constituents were associated with adverse respiratory effects (2)(3)(4). Although traffic emissions remain the primary source of PAHs in United States cities, PAHs are also emitted readily from industrial sources, cigarette smoke, incense burning, cooking, and space heating (5,6).…”

“…Although traffic emissions remain the primary source of PAHs in United States cities, PAHs are also emitted readily from industrial sources, cigarette smoke, incense burning, cooking, and space heating (5,6). Previous work by the Columbia Center for Children's Environmental Health (CCCEH) and others linked exposure to ambient PAHs in particular with asthma-like symptoms in young children and with seroatopy (2,7,8). However, the mechanism responsible for these findings has not been elucidated.…”

Endotoxin in inner-city homes: Associations with wheeze and eczema in early childhood

“…Participants included 301 children recruited as part of an ongoing birth cohort, described previously, being conducted by Columbia's Center for Children's Environmental Health (14)(15)(16)(17). Non-smoking mothers not selected on allergic/asthmatic status of African-American and Dominican ethnicity living in Northern Manhattan and the South Bronx were recruited during the second or third trimester of pregnancy from prenatal clinics.…”