Prenatal Air Pollution Exposure and Newborn Blood Pressure

Background

Air pollution exposure has been associated with increased blood pressure in adults.

Objective:

We examined associations of antenatal exposure to ambient air pollution with newborn systolic blood pressure (SBP).

Methods:

We studied 1,131 mother–infant pairs in a Boston, Massachusetts, area pre-birth cohort. We calculated average exposures by trimester and during the 2 to 90 days before birth for temporally resolved fine particulate matter (≤ 2.5 μm; PM_2.5), black carbon (BC), nitrogen oxides, nitrogen dioxide, ozone (O₃), and carbon monoxide measured at stationary monitoring sites, and for spatiotemporally resolved estimates of PM_2.5 and BC at the residence level. We measured SBP at a mean age of 30 ± 18 hr with an automated device. We used mixed-effects models to examine associations between air pollutant exposures and SBP, taking into account measurement circumstances; child’s birth weight; mother’s age, race/ethnicity, socioeconomic position, and third-trimester BP; and time trend. Estimates represent differences in SBP associated with an interquartile range (IQR) increase in each pollutant.

Results:

Higher mean PM_2.5 and BC exposures during the third trimester were associated with higher SBP (e.g., 1.0 mmHg; 95% CI: 0.1, 1.8 for a 0.32-μg/m³ increase in mean 90-day residential BC). In contrast, O₃ was negatively associated with SBP (e.g., –2.3 mmHg; 95% CI: –4.4, –0.2 for a 13.5-ppb increase during the 90 days before birth).

Conclusions:

Exposures to PM_2.5 and BC in late pregnancy were positively associated with newborn SBP, whereas O₃ was negatively associated with SBP. Longitudinal follow-up will enable us to assess the implications of these findings for health during later childhood and adulthood.

Citation:

van Rossem L, Rifas-Shiman SL, Melly SJ, Kloog I, Luttmann-Gibson H, Zanobetti A, Coull BA, Schwartz JD, Mittleman MA, Oken E, Gillman MW, Koutrakis P, Gold DR. 2015. Prenatal air pollution exposure and newborn blood pressure. Environ Health Perspect 123:353–359; http://dx.doi.org/10.1289/ehp.1307419     

High Blood Pressure and Long-Term Exposure to Indoor Noise and Air Pollution from Road Traffic

Background: Traffic noise has been associated with prevalence of hypertension, but reports are inconsistent for blood pressure (BP). To ascertain noise effects and to disentangle them from those suspected to be from traffic-related air pollution, it may be essential to estimate people’s noise exposure indoors in bedrooms.Objectives: We analyzed associations between long-term exposure to indoor traffic noise in bedrooms and prevalent hypertension and systolic (SBP) and diastolic (DBP) BP, considering long-term exposure to outdoor nitrogen dioxide (NO₂).Methods: We evaluated 1,926 cohort participants at baseline (years 2003–2006; Girona, Spain). Outdoor annual average levels of nighttime traffic noise (L_night) and NO₂ were estimated at postal addresses with a detailed traffic noise model and a land-use regression model, respectively. Individual indoor traffic L_night levels were derived from outdoor L_night with application of insulations provided by reported noise-reducing factors. We assessed associations for hypertension and BP with multi-exposure logistic and linear regression models, respectively.Results: Median levels were 27.1 dB(A) (indoor L_night), 56.7 dB(A) (outdoor L_night), and 26.8 μg/m³ (NO₂). Spearman correlations between outdoor and indoor L_night with NO₂ were 0.75 and 0.23, respectively. Indoor L_night was associated both with hypertension (OR = 1.06; 95% CI: 0.99, 1.13) and SBP (β = 0.72; 95% CI: 0.29, 1.15) per 5 dB(A); and NO₂ was associated with hypertension (OR = 1.16; 95% CI: 0.99, 1.36), SBP (β = 1.23; 95% CI: 0.21, 2.25), and DBP (β⊇= 0.56; 95% CI: –0.03, 1.14) per 10 μg/m³. In the outdoor noise model, L_night was associated only with hypertension and NO₂ with BP only. The indoor noise–SBP association was stronger and statistically significant with a threshold at 30 dB(A).Conclusion: Long-term exposure to indoor traffic noise was associated with prevalent hypertension and SBP, independently of NO₂. Associations were less consistent for outdoor traffic L_night and likely affected by collinearity.Citation: Foraster M, Künzli N, Aguilera I, Rivera M, Agis D, Vila J, Bouso L, Deltell A, Marrugat J, Ramos R, Sunyer J, Elosua R, Basagaña X. 2014. High blood pressure and long-term exposure to indoor noise and air pollution from road traffic. Environ Health Perspect 122:1193–1200; http://dx.doi.org/10.1289/ehp.1307156     

Arterial Blood Pressure and Long-Term Exposure to Traffic-Related Air Pollution: An Analysis in the European Study of Cohorts for Air Pollution Effects (ESCAPE)

Background: Long-term exposure to air pollution has been hypothesized to elevate arterial blood pressure (BP). The existing evidence is scarce and country specific.Objectives: We investigated the cross-sectional association of long-term traffic-related air pollution with BP and prevalent hypertension in European populations.Methods: We analyzed 15 population-based cohorts, participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE). We modeled residential exposure to particulate matter and nitrogen oxides with land use regression using a uniform protocol. We assessed traffic exposure with traffic indicator variables. We analyzed systolic and diastolic BP in participants medicated and nonmedicated with BP-lowering medication (BPLM) separately, adjusting for personal and area-level risk factors and environmental noise. Prevalent hypertension was defined as ≥ 140 mmHg systolic BP, or ≥ 90 mmHg diastolic BP, or intake of BPLM. We combined cohort-specific results using random-effects meta-analysis.Results: In the main meta-analysis of 113,926 participants, traffic load on major roads within 100 m of the residence was associated with increased systolic and diastolic BP in nonmedicated participants [0.35 mmHg (95% CI: 0.02, 0.68) and 0.22 mmHg (95% CI: 0.04, 0.40) per 4,000,000 vehicles × m/day, respectively]. The estimated odds ratio (OR) for prevalent hypertension was 1.05 (95% CI: 0.99, 1.11) per 4,000,000 vehicles × m/day. Modeled air pollutants and BP were not clearly associated.Conclusions: In this first comprehensive meta-analysis of European population-based cohorts, we observed a weak positive association of high residential traffic exposure with BP in nonmedicated participants, and an elevated OR for prevalent hypertension. The relationship of modeled air pollutants with BP was inconsistent.Citation: Fuks KB, Weinmayr G, Foraster M, Dratva J, Hampel R, Houthuijs D, Oftedal B, Oudin A, Panasevich S, Penell J, Sommar JN, Sørensen M, Tittanen P, Wolf K, Xun WW, Aguilera I, Basagaña X, Beelen R, Bots ML, Brunekreef B, Bueno-de-Mesquita HB, Caracciolo B, Cirach M, de Faire U, de Nazelle A, Eeftens M, Elosua R, Erbel R, Forsberg B, Fratiglioni L, Gaspoz JM, Hilding A, Jula A, Korek M, Krämer U, Künzli N, Lanki T, Leander K, Magnusson PK, Marrugat J, Nieuwenhuijsen MJ, Östenson CG, Pedersen NL, Pershagen G, Phuleria HC, Probst-Hensch NM, Raaschou-Nielsen O, Schaffner E, Schikowski T, Schindler C, Schwarze PE, Søgaard AJ, Sugiri D, Swart WJ, Tsai MY, Turunen AW, Vineis P, Peters A, Hoffmann B. 2014. Arterial blood pressure and long-term exposure to traffic-related air pollution: an analysis in the European Study of Cohorts for Air Pollution Effects (ESCAPE). Environ Health Perspect 122:896–905; http://dx.doi.org/10.1289/ehp.1307725     

Association between Long-Term Exposure to Traffic-Related Air Pollution and Subclinical Atherosclerosis: The REGICOR Study

Background: Epidemiological evidence of the effects of long-term exposure to air pollution on the chronic processes of atherogenesis is limited.Objective: We investigated the association of long-term exposure to traffic-related air pollution with subclinical atherosclerosis, measured by carotid intima media thickness (IMT) and ankle–brachial index (ABI).Methods: We performed a cross-sectional analysis using data collected during the reexamination (2007–2010) of 2,780 participants in the REGICOR (Registre Gironí del Cor: the Gerona Heart Register) study, a population-based prospective cohort in Girona, Spain. Long-term exposure across residences was calculated as the last 10 years’ time-weighted average of residential nitrogen dioxide (NO₂) estimates (based on a local-scale land-use regression model), traffic intensity in the nearest street, and traffic intensity in a 100 m buffer. Associations with IMT and ABI were estimated using linear regression and multinomial logistic regression, respectively, controlling for sex, age, smoking status, education, marital status, and several other potential confounders or intermediates.Results: Exposure contrasts between the 5th and 95th percentiles for NO₂ (25 µg/m³), traffic intensity in the nearest street (15,000 vehicles/day), and traffic load within 100 m (7,200,000 vehicle-m/day) were associated with differences of 0.56% (95% CI: –1.5, 2.6%), 2.32% (95% CI: 0.48, 4.17%), and 1.91% (95% CI: –0.24, 4.06) percent difference in IMT, respectively. Exposures were positively associated with an ABI of > 1.3, but not an ABI of < 0.9. Stronger associations were observed among those with a high level of education and in men ≥ 60 years of age.Conclusions: Long-term traffic-related exposures were associated with subclinical markers of atherosclerosis. Prospective studies are needed to confirm associations and further examine differences among population subgroups.     

Carotid Intima-Media Thickness and Long-Term Exposure to Traffic-Related Air Pollution in Middle-Aged Residents of Taiwan: A Cross-Sectional Study

Background

Associations between long-term exposure to air pollution and carotid intima-media thickness (CIMT) have inconsistent findings.

Objectives

In this study we aimed to evaluate association between 1-year average exposure to traffic-related air pollution and CIMT in middle-aged adults in Asia.

Methods

CIMT was measured in Taipei, Taiwan, between 2009 and 2011 in 689 volunteers 35–65 years of age who were recruited as the control subjects of an acute coronary heart disease cohort study. We applied land-use regression models developed by the European Study of Cohorts for Air Pollution Effects (ESCAPE) to estimate each subject’s 1-year average exposure to traffic-related air pollutants with particulate matter diameters ≤ 10 μm (PM₁₀) and ≤ 2.5 μm (PM_2.5) and the absorbance levels of PM_2.5 (PM_2.5abs), nitrogen dioxide (NO₂), and nitrogen oxides (NO_x) in the urban environment.

Results

One-year average air pollution exposures were 44.21 ± 4.19 μg/m³ for PM₁₀, 27.34 ± 5.12 μg/m³ for PM_2.5, and (1.97 ± 0.36) × 10^–5/m for PM_2.5abs. Multivariate regression analyses showed average percentage increases in maximum left CIMT of 4.23% (95% CI: 0.32, 8.13) per 1.0 × 10^–5/m increase in PM_2.5abs; 3.72% (95% CI: 0.32, 7.11) per 10-μg/m³ increase in PM₁₀; 2.81% (95% CI: 0.32, 5.31) per 20-μg/m³ increase in NO₂; and 0.74% (95% CI: 0.08, 1.41) per 10-μg/m³ increase in NO_x. The associations were not evident for right CIMT, and PM_2.5 mass concentration was not associated with the outcomes.

Conclusions

Long-term exposures to traffic-related air pollution of PM_2.5abs, PM₁₀, NO₂, and NO_x were positively associated with subclinical atherosclerosis in middle-aged adults.

Citation

Su TC, Hwang JJ, Shen YC, Chan CC. 2015. Carotid intima–media thickness and long-term exposure to traffic-related air pollution in middle-aged residents of Taiwan: a cross-sectional study. Environ Health Perspect 123:773–778; http://dx.doi.org/10.1289/ehp.1408553     

农村地区空气污染人群暴露评价研究

目的了解我国农村欠发达地区空气污染的状况及农村人群对空气污染的实际暴露水平。方法选择安庆市所属两个县18个乡镇的189个家庭,对其室内、外空气污染水平进行环境监测 ,同时对上述家庭中年龄在15～65岁之间的488名调查对象进行入户问卷调查。结果被调查地区存在严重的室内外空气污染 ,污染物以可吸入颗粒物PM10 为主 ,厨房、卧室、庭院、田间分别为(518±27)μg/m3,(340±9)μg/m3,(287±9)μg/m3,(270±10)μg/m3,室内污染水平显著高于室外 (P<0.01) ;SO2 和CO的污染水平较低 (P>0.05)。结合个体暴露时间和环境暴露浓度对个体的综合空气污染暴露进行综合评价的结果显示 ,该地区农村居民冬季对PM10 的实际暴露水平明显高于国家卫生标准 ,而其室内外空气污染主要来源是由于做饭和取暖的燃料燃烧引起。结论该地区农村室内空气污染严重 ,污染物以PM10 为主     

Associations between Long-Term Air Pollutant Exposures and Blood Pressure in Elderly Residents of Taipei City: A Cross-Sectional Study

Background

Limited information is available regarding long-term effects of air pollution on blood pressure (BP) and hypertension.

Objective

We studied whether 1-year exposures to particulate matter (PM) and nitrogen oxides (NO_x) were correlated with BP and hypertension in the elderly.

Methods

We analyzed cross-sectional data from 27,752 Taipei City residents > 65 years of age who participated in a health examination program in 2009. Land-use regression models were used to estimate participants’ 1-year exposures to particulate matter with aerodynamic diameter ≤ 10 μm (PM₁₀), coarse particles (PM_2.5–10), fine particles (≤ 2.5 μm; PM_2.5), PM_2.5 absorbance, NO_x, and nitrogen dioxide (NO₂). Generalized linear regressions and logistic regressions were used to examine the association between air pollution and BP and hypertension, respectively.

Results

Diastolic BP was associated with 1-year exposures to air pollution, with estimates of 0.73 [95% confidence interval (CI): 0.44, 1.03], 0.46 (95% CI: 0.30, 0.63), 0.62 (95% CI: 0.24, 0.99), 0.34 (95% CI: 0.19, 0.50), and 0.65 (95% CI: 0.44, 0.85) mmHg for PM₁₀ (10 μg/m³), PM_2.5–10 (5 μg/m³), PM_2.5 absorbance (10^–5/m), NO_x (20 μg/m³), and NO₂ (10 μg/m³), respectively. PM_2.5 was not associated with diastolic BP, and none of the air pollutants was associated with systolic BP. Associations of diastolic BP with PM₁₀ and PM_2.5 absorbance were stronger among participants with hypertension, diabetes, or a body mass index ≥ 25 kg/m² than among participants without these conditions. One-year air pollution exposures were not associated with hypertension.

Conclusions

One-year exposures to PM₁₀, PM_2.5–10, PM_2.5 absorbance, and NO_x were associated with higher diastolic BP in elderly residents of Taipei.

Citation

Chen SY, Wu CF, Lee JH, Hoffmann B, Peters A, Brunekreef B, Chu DC, Chan CC. 2015. Associations between long-term air pollutant exposures and blood pressure in elderly residents of Taipei City: a cross-sectional study. Environ Health Perspect 123:779–784; http://dx.doi.org/10.1289/ehp.1408771     

Importance of the Indoor Environment in Air Pollution Exposure

A portable personal air pollution sampler was used to measure the exposure of twenty children to respirable particulates, sulfur dioxide, and nitrogen dioxide over a 24-hour period. Particulate exposures were significantly higher among children who lived with one or more smokers, and exceeded the primary air quality standard in nineteen of the twenty subjects. To a large extent, an individual’s respirable particulate load appears to be determined by exposure to indoor rather than outdoor pollutants.     

Long-Term Exposure to Urban Air Pollution and Mortality in a Cohort of More than a Million Adults in Rome

Background: Few European studies have investigated the effects of long-term exposure to both fine particulate matter (≤ 2.5 µm; PM_2.5) and nitrogen dioxide (NO₂) on mortality.Objectives: We studied the association of exposure to NO₂, PM_2.5, and traffic indicators on cause-specific mortality to evaluate the form of the concentration–response relationship.Methods: We analyzed a population-based cohort enrolled at the 2001 Italian census with 9 years of follow-up. We selected all 1,265,058 subjects ≥ 30 years of age who had been living in Rome for at least 5 years at baseline. Residential exposures included annual NO₂ (from a land use regression model) and annual PM_2.5 (from a Eulerian dispersion model), as well as distance to roads with > 10,000 vehicles/day and traffic intensity. We used Cox regression models to estimate associations with cause-specific mortality adjusted for individual (sex, age, place of birth, residential history, marital status, education, occupation) and area (socioeconomic status, clustering) characteristics.Results: Long-term exposures to both NO₂ and PM_2.5 were associated with an increase in nonaccidental mortality [hazard ratio (HR) = 1.03 (95% CI: 1.02, 1.03) per 10-µg/m³ NO₂; HR = 1.04 (95% CI: 1.03, 1.05) per 10-µg/m³ PM_2.5]. The strongest association was found for ischemic heart diseases (IHD) [HR = 1.10 (95% CI: 1.06, 1.13) per 10-µg/m³ PM_2.5], followed by cardiovascular diseases and lung cancer. The only association showing some deviation from linearity was that between NO₂ and IHD. In a bi-pollutant model, the estimated effect of NO₂ on mortality was independent of PM_2.5.Conclusions: This large study strongly supports an effect of long-term exposure to NO₂ and PM_2.5 on mortality, especially from cardiovascular causes. The results are relevant for the next European policy decisions regarding air quality.     

Controlled Exposure Study of Air Pollution and T-Wave Alternans in Volunteers without Cardiovascular Disease

Background: Epidemiological studies have assessed T-wave alternans (TWA) as a possible mechanism of cardiac arrhythmias related to air pollution in high-risk subjects and have reported associations with increased TWA magnitude.Objective: In this controlled human exposure study, we assessed the impact of exposure to concentrated ambient particulate matter (CAP) and ozone (O3) on T-wave alternans in resting volunteers without preexisting cardiovascular disease.Methods: Seventeen participants without preexisting cardiovascular disease were randomized to filtered air (FA), CAP (150 μg/m3), O3 (120 ppb), or combined CAP + O3 exposures for 2 hr. Continuous electrocardiograms (ECGs) were recorded at rest and T-wave alternans (TWA) was computed by modified moving average analysis with QRS alignment for the artifact-free intervals of 20 beats along the V2 and V5 leads. Exposure-induced changes in the highest TWA magnitude (TWAMax) were estimated for the first and last 5 min of each exposure (TWAMax_Early and TWAMax_Late respectively). ΔTWAMax (Late-Early) were compared among exposure groups using analysis of variance.Results: Mean ± SD values for ΔTWAMax were -2.1 ± 0.4, -2.7 ± 1.1, -1.9 ± 1.5, and -1.2 ± 1.5 in FA, CAP, O3, and CAP + O3 exposure groups, respectively. No significant differences were observed between pollutant exposures and FA.Conclusion: In our study of 17 volunteers who had no preexisting cardiovascular disease, we did not observe significant changes in T-wave alternans after 2-hr exposures to CAP, O3, or combined CAP + O3. This finding, however, does not preclude the possibility of pollution-related effects on TWA at elevated heart rates, such as during exercise, or the possibility of delayed responses.     

Long-Term Exposure to Ambient Air Pollution and Incidence of Cerebrovascular Events: Results from 11 European Cohorts within the ESCAPE Project

Background: Few studies have investigated effects of air pollution on the incidence of cerebrovascular events.Objectives: We assessed the association between long-term exposure to multiple air pollutants and the incidence of stroke in European cohorts.Methods: Data from 11 cohorts were collected, and occurrence of a first stroke was evaluated. Individual air pollution exposures were predicted from land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE). The exposures were: PM_2.5 [particulate matter (PM) ≤ 2.5 μm in diameter], coarse PM (PM between 2.5 and 10 μm), PM₁₀ (PM ≤ 10 μm), PM_2.5 absorbance, nitrogen oxides, and two traffic indicators. Cohort-specific analyses were conducted using Cox proportional hazards models. Random-effects meta-analysis was used for pooled effect estimation.Results: A total of 99,446 study participants were included, 3,086 of whom developed stroke. A 5-μg/m³ increase in annual PM_2.5 exposure was associated with 19% increased risk of incident stroke [hazard ratio (HR) = 1.19, 95% CI: 0.88, 1.62]. Similar findings were obtained for PM₁₀. The results were robust to adjustment for an extensive list of cardiovascular risk factors and noise coexposure. The association with PM_2.5 was apparent among those ≥ 60 years of age (HR = 1.40, 95% CI: 1.05, 1.87), among never-smokers (HR = 1.74, 95% CI: 1.06, 2.88), and among participants with PM_2.5 exposure < 25 μg/m³ (HR = 1.33, 95% CI: 1.01, 1.77).Conclusions: We found suggestive evidence of an association between fine particles and incidence of cerebrovascular events in Europe, even at lower concentrations than set by the current air quality limit value.Citation: Stafoggia M, Cesaroni G, Peters A, Andersen ZJ, Badaloni C, Beelen R, Caracciolo B, Cyrys J, de Faire U, de Hoogh K, Eriksen KT, Fratiglioni L, Galassi C, Gigante B, Havulinna AS, Hennig F, Hilding A, Hoek G, Hoffmann B, Houthuijs D, Korek M, Lanki T, Leander K, Magnusson PK, Meisinger C, Migliore E, Overvad K, Östenson CG, Pedersen NL, Pekkanen J, Penell J, Pershagen G, Pundt N, Pyko A, Raaschou-Nielsen O, Ranzi A, Ricceri F, Sacerdote C, Swart WJ, Turunen AW, Vineis P, Weimar C, Weinmayr G, Wolf K, Brunekreef B, Forastiere F. 2014. Long-term exposure to ambient air pollution and incidence of cerebrovascular events: results from 11 European cohorts within the ESCAPE project. Environ Health Perspect 122:919–925; http://dx.doi.org/10.1289/ehp.1307301     

Blood Pressure Changes and Chemical Constituents of Particulate Air Pollution: Results from the Healthy Volunteer Natural Relocation (HVNR) Study

Background: Elevated blood pressure (BP) has been associated with particulate matter (PM) air pollution, but associations with PM chemical constituents are still uncertain.Objectives: We investigated associations of BP with various chemical constituents of fine PM (PM_2.5) during 460 repeated visits among a panel of 39 university students.Methods: Resting BP was measured using standardized methods before and after the university students relocated from a suburban campus to an urban campus with different air pollution contents in Beijing, China. Air pollution data were obtained from central monitors close to student residences. We used mixed-effects models to estimate associations of various PM_2.5 constituents with systolic BP (SBP), diastolic BP (DBP), and pulse pressure.Results: An interquartile range increase of 51.2 μg/m³ in PM_2.5 was associated with a 1.08-mmHg (95% CI: 0.17, 1.99) increase in SBP and a 0.96-mmHg (95% CI: 0.31, 1.61) increase in DBP on the following day. A subset of PM_2.5 constituents, including carbonaceous fractions (organic carbon and elemental carbon), ions (chloride and fluoride), and metals/metalloid elements (nickel, zinc, magnesium, lead, and arsenic), were found to have robust positive associations with different BP variables, though robust negative associations of manganese, chromium, and molybdenum with SBP or DBP also were observed.Conclusions: Our results support relationships between specific PM_2.5 constituents and BP. These findings have potential implications for the development of pollution abatement strategies that maximize public health benefits.     

Air Pollution Exposure and Markers of Placental Growth and Function: The Generation R Study

Background: Air pollution exposure during pregnancy might affect placental growth and function, perhaps leading to pregnancy complications.Objective: We prospectively evaluated the associations of maternal air pollution exposure with markers of placental growth and function among 7,801 pregnant women in the Netherlands.Methods: We estimated levels of particulate matter ≤ 10 µm in aerodynamic diameter (PM₁₀) and nitrogen dioxide (NO₂) at the home address for different periods during pregnancy using dispersion modeling techniques. Pro- and anti-angiogenic factors [placental growth factor (PlGF) and soluble fms-like tyrosine kinase 1 (sFlt-1), respectively] were measured in first- and second-trimester maternal blood and in fetal cord blood samples at delivery. Pulsatility index of the uterine and umbilical arteries was measured by Doppler ultrasound in second and third trimester, and notching was assessed in third trimester. Placenta weight and birth weight were obtained from medical records.Results: Higher PM₁₀ and NO₂ exposure levels were associated with lower second-trimester maternal sFlt-1 and PlGF levels. PM₁₀ and NO₂ exposures averaged over total pregnancy were associated with higher sFlt-1 and lower PlGF levels in fetal cord blood, consistent with an anti-angiogenic state. PM₁₀ and NO₂ exposures were not consistently associated with second- or third-trimester placental resistance indices. NO₂ exposure was associated with third-trimester notching (odds ratio 1.33; 95% CI: 0.99, 1.78 per 10-µg/m³ increase in the prior 2 months). PM₁₀ and NO₂ exposures were associated with lower placenta weight (–11.8 g; 95% CI: –20.9, –2.7, and –10.7 g; 95% CI: –19.0, –2.4, respectively, per 10-µg/m³ increase in the prior 2 months), but not with placenta to birth weight ratio.Conclusions: Our results suggest that maternal air pollution exposure may influence markers of placental growth and function. Future studies are needed to confirm these findings and explore the maternal and fetal consequences.