Variability of total exposure to PM2.5 related to indoor and outdoor pollution sources

Environment International

Spengler²

2014

Objectives Relative importance of multiple indoor and outdoor venues on personal exposure concentrations to pro-carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) remains poorly understood. This is particularly challenging because many c-PAHs share sources and occur as a complex mixture. Accurate and precise apportionment of personal exposure according to exposure venues could aid in understanding of human health effects due to given source. Here, we partitioned indoor and personal exposure concentrations to seven c-PAHs and pyrene according to the indoor- and outdoor- origins. Methods A simultaneous, integrated monitoring of personal, indoor and outdoor concentrations of nine PAHs was conducted in 75 homes for a consecutive 48-hour period across a two-year period in Kraków, Poland. Due to few known indoor sources for chrysene, we used this PAH species as a tracer for infiltration of outdoor PAHs. Personal and indoor concentrations of seven c-PAHs and pyrene were apportioned to home indoor, non-home indoor and outdoor origin. Results Using Chrysenein / Chryseneout as proxy for an infiltration factor, Finf, infiltrated PAHs of outdoor origin are overall higher in concentration than those emitted from the indoor origin. Average contribution by the outdoor sources on B[a]A, B[b]F, and B[k]F were 92%, 79%, and 78% across all seasons. In contrast, in homes where a household members smoked, average contribution by the outdoor sources on B[ghi]P, B[a]P, D[ah]A, and IP were lower (i.e., 67%, 65%, 67%, and 66%, respectively). Season-averaged contribution by the outdoor sources on personal exposure to B[a]A, B[b]F, and B[k]F were 92%, 74%, and 77%, respectively. On the other hand, season-averaged home indoor source contribution on personal exposure to B[a]A, B[b]F, and B[k]F were estimated at 6%, 15%, and 19%, respectively. Similar contributions by season-averaged home indoor sources on personal exposure were estimated at 28% for B[ghi]P, 31% for B[a]P, 25% for D[ah]A, and 28% for IP. Conclusion Of the seven c-PAHs, B[a]A, B[b]F, and B[k]F are enriched in indoor and personal exposure concentrations from the outdoor coal-combustion. B[ghi]P, B[a]P, D[a,h]A, and IP, PAHs with some of the highest carcinogenic and mutagenic potencies, are considerably enriched by cigarette smoke in addition to the outdoor sources.

“…Details on the subject enrollment and air monitoring methods have been published (Choi et al, 2006; Jedrychowski et al, 2004; Jedrychowski et al, 2006) and briefly summarized below.…”

Section: Methodsmentioning

confidence: 99%

Source attribution of personal exposure to airborne polycyclic aromatic hydrocarbon mixture using concurrent personal, indoor, and outdoor measurements

Environment International

Spengler²

2014

“…Details on study design for the Krakow cohort have been previously published (Jedrychowski et al 2004, 2006). Nonsmoking, pregnant women residing in the Srodmiescie (Old Podgorze) and the Krowodrza-Nowa Huta (New Podgorze) areas were recruited between November 2000 and March 2003 (Jedrychowski et al 2004).…”

Section: Methodsmentioning

confidence: 99%

“…Details of the personal air monitoring conducted in Krakow (Jedrychowski et al 2004, 2006) and NYC (Perera et al 2003; Tonne et al 2004) have been published. Briefly, on completion of the interview, the women were given a backpack containing a portable personal exposure air monitor to be worn during the day and kept near the bed at night during a consecutive 48-hr period.…”

Section: Methodsmentioning

confidence: 99%

International Studies of Prenatal Exposure to Polycyclic Aromatic Hydrocarbons and Fetal Growth

Environ Health Perspect

Jędrychowski

Spengler³

et al. 2006

Self Cite

236

217

ObjectivesPolycyclic aromatic hydrocarbons (PAHs) are ubiquitously distributed human mutagens and carcinogens. However, lack of adequate air monitoring data has limited understanding of the effects of airborne PAHs on fetal growth. To address this gap in knowledge, we examined the association between prenatal exposure to airborne PAHs and birth weight, birth length, and birth head circumference, respectively, in Krakow, Poland, and New York City (NYC).MethodsThe parallel prospective cohort studies enrolled nonsmoking, healthy, and nonoccupationally exposed women and their newborns. Personal air monitoring of pregnant women was conducted over 48 hr. To control for maternal environmental tobacco smoke (ETS) exposure, we excluded those with umbilical cord plasma cotinine concentrations > 25 ng/mL. Mean cord plasma cotinine concentrations in both ethnic groups were ≤ 0.5 ng/mL.ResultsPrenatal PAH exposure was 10-fold higher in Krakow than in NYC. Prenatal PAH exposure was associated with significantly reduced birth weight in both Krakow Caucasians (p < 0.01) and in NYC African Americans (p < 0.01), controlling for known and potential confounders, but not in NYC Dominicans. Within the lower exposure range common to the two cities (1.80–36.47 ng/m3), the effect per unit PAH exposure on birth weight was 6-fold greater for NYC African Americans than for Krakow Caucasians (p = 0.01).ConclusionsThese results confirm the adverse reproductive effect of relatively low PAH concentrations in two populations and suggest increased susceptibility of NYC African Americans. Fetal growth impairment has been linked to child developmental and health problems. Thus, substantial health benefits would result from global reduction of PAH emissions.

“…For example, personal exposure to the sum of eight carcinogenic PAHs (∑8c-PAHs) in Krakow, Poland, varies by > 10-fold across seasons (Choi et al 2006). In addition, mean personal exposure to PM 2.5 for women monitored during the heating season was significantly higher than for women monitored during the nonheating season (43.37 vs. 29.77 μg/m 3 , p < 0.001) (Jedrychowski et al 2006). …”

mentioning

confidence: 99%

“…The present analysis is part of an ongoing prospective cohort study on prenatal and early childhood exposure to multiple toxicants on a number of developmental and health outcomes (Choi et al 2006; Jedrychowski et al 2004, 2005a, 2005b, 2006). Here, we focus on developing a gestation-length model of personal exposure to ∑8c-PAH among pregnant women enrolled in an ongoing study in Krakow.…”

mentioning

confidence: 99%

Estimating Individual-Level Exposure to Airborne Polycyclic Aromatic Hydrocarbons throughout the Gestational Period Based on Personal, Indoor, and Outdoor Monitoring

Environ Health Perspect

Perera

Pac

et al. 2008

Self Cite

ObjectivesCurrent understanding on health effects of long-term polycyclic aromatic hydrocarbon (PAH) exposure is limited by lack of data on time-varying nature of the pollutants at an individual level. In a cohort of pregnant women in Krakow, Poland, we examined the contribution of temporal, spatial, and behavioral factors to prenatal exposure to airborne PAHs within each trimester and developed a predictive model of PAH exposure over the entire gestational period.MethodsWe monitored nonsmoking pregnant women (n = 341) for their personal exposure to pyrene and eight carcinogenic PAHs—benz[a]anthracene, chrysene/isochrysene, benzo[b]fluoranthene, benzo[k]fluoranthene, benzo[a]pyrene [B(a)P], indeno[1,2,3-c,d]pyrene, dibenz[a,h]anthracene, and benzo[g,h,i]perylene—during their second trimester for a consecutive 48-hr period. In a subset (n = 78), we monitored indoor and outdoor levels simultaneously with the personal monitoring during the second trimester with an identical monitor. The subset of women was also monitored for personal exposure for a 48-hr period during each trimester. We repeatedly administered a questionnaire on health history, lifestyle, and home environment.ResultsThe observed personal, indoor, and outdoor B(a)P levels we observed in Krakow far exceed the recommended Swedish guideline value for B(a)P of 0.1 ng/m3. Based on simultaneously monitored levels, the outdoor PAH level alone accounts for 93% of total variability in personal exposure during the heating season. Living near the Krakow bus depot, a crossroad, and the city center and time spent outdoors or commuting were not associated with higher personal exposure. During the nonheating season only, a 1-hr increase in environmental tobacco smoke (ETS) exposure was associated with a 10–16% increase in personal exposure to the nine measured PAHs. A 1°C decrease in ambient temperature was associated with a 3–5% increase in exposure to benz[a]anthracene, benzo[k]fluoranthene, and dibenz[a,h]anthracene, after accounting for the outdoor concentration. A random effects model demonstrated that mean personal exposure at a given gestational period depends on the season, residence location, and ETS.ConclusionConsidering that most women reported spending < 3 hr/day outdoors, most women in the study were exposed to outdoor-originating PAHs within the indoor setting. Cross-sectional, longitudinal monitoring supplemented with questionnaire data allowed development of a gestation-length model of individual-level exposure with high precision and validity. These results are generalizable to other nonsmoking pregnant women in similar exposure settings and support reduction of exposure to protect the developing fetus.