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Over the last decades many epidemiologic studies considered the morbidity patterns for respiratory diseases and lung function of children in the context of ambient air pollution usually measured in the postnatal period. The main purpose of this study is to assess the impact of prenatal exposure to fine particulate matter (PM2.5) on the recurrent broncho-pulmonary infections in early childhood.
The study included 214 children who had measurements of personal prenatal PM2.5 exposure and regularly collected data on the occurrence of acute bronchitis and pneumonia diagnosed by a physician from birth over the seven-year follow-up. The effect of prenatal exposure to PM2.5 was adjusted in the multivariable logistic models for potential confounders, such as prenatal and postnatal ETS (environmental tobacco smoke), city residence area as a proxy of postnatal urban exposure, children’s sensitization to domestic aeroallergens, and asthma. In the subgroup of children with available PM2.5 indoor levels, the effect of prenatal exposure was additionally adjusted for indoor exposure as well. The adjusted odds ratio (OR) for incidence of recurrent broncho-pulmonary infections (five or more spells of bronchitis and/or pneumonia) recorded in the follow-up significantly correlated in a dose-response manner with the prenatal PM2.5 level (OR = 2.44, 95%CI: 1.12 – 5.36).
In conclusion, the study suggests that prenatal exposure to PM2.5 increases susceptibility to respiratory infections and may program respiratory morbidity in early childhood. The study also provides evidence that the target value of 20 μg/m3 for the 24-hour mean level of PM2.5 protects unborn babies better than earlier established EPA guidelines.
PMCID: PMC3657308  PMID: 23333083
birth cohort study; fine particulate matter; prenatal and postnatal exposure; bronchitis; pneumonia
2.  Gender differences in fetal growth of newborns exposed prenatally to airborne fine particulate matter 
Environmental research  2009;109(4):447-456.
Our primary purpose was to assess sex-specific fetal growth reduction in newborns exposed prenatally to fine particulate matter. Only women 18–35 years of age, who claimed to be non-smokers, with singleton pregnancies, without illicit drug use and HIV infection, free from chronic diseases were eligible for the study. A total of 481 enrolled pregnant women who gave birth between 37 and 43 weeks of gestation were included in the study. Prenatal personal exposure to fine particles over 48 h during the second trimester was measured using personal monitors. To evaluate the relationship between the level of PM2.5 measured over 48 h in the second trimester of pregnancy with those in the first and the third trimesters, a series of repeated measurements in each trimester was carried out in a random subsample of 85 pregnant women. We assessed the effect of PM2.5 exposure on the birth outcomes (weight, length and head circumference at birth) by multivariable regression models, controlling for potential confounders (maternal education, gestational age, parity, maternal height and prepregnancy weight, sex of infant, prenatal environmental tobacco smoke, and season of birth). Birth outcomes were associated positively with gestational age, parity, maternal height and prepregnancy weight, but negatively with the level of prenatal PM2.5 exposure. Overall average increase in gestational period of prenatal exposure to fine particles by about 30 μg/m3, i.e., from 25th percentile (23.4 μg/m3) to 75th percentile (53.1 μg/m3) brought about an average birth weight deficit of 97.2 g (95% CI: −201, 6.6) and length at birth of 0.7cm (95% CI: −1.36, −0.04). The corresponding exposure lead to birth weight deficit in male newborns of 189 g (95% CI: −34.2, −343) in comparison to 17 g in female newborns; the deficit of length at birth in male infants amounted to 1.1 cm (95% CI: −0.11, −2.04). We found a significant interrelationship between self-reported ETS and PM2.5, however, none of the models showed a significant interaction of both variables. The joint effect of various levels of PM2.5 and ETS on birth outcomes showed the significant deficit only for the categories of exposure with higher component of PM2.5. Concluding, the results of the study suggest that observed deficits in birth outcomes are rather attributable to prenatal PM2.5 exposure and not to environmental tobacco smoke. The study also provided evidence that male fetuses are more sensitive to prenatal PM2.5 exposure and this should persuade policy makers to consider birth outcomes by gender separately while setting air pollution guidelines.
PMCID: PMC3786262  PMID: 19261271
Cohort study; Prenatal exposure; Air pollutants; Fine particles; Gender; Fetal growth deficits
In a birth cohort study, we have assessed the dose-response relationship between individual measurements of prenatal airborne PAH exposure and specific PAH-DNA adducts in cord blood adjusted for maternal blood adducts and season of birth. The study uses data from an earlier established birth cohort of children in Krakow. The final analysis included 362 pregnant women who gave birth to term babies and had complete data on personal exposure in the second trimester of pregnancy to eight airborne polycyclic aromatic hydrocarbons (PAH) including benzo[a]pyrene (B[a]P), as well as DNA adducts, both in maternal and cord blood.
The relation between cord blood PAH-DNA adducts and airborne prenatal PAH exposure was non-linear. While cord blood PAH-DNA adducts were significantly associated with the B[a]P exposure categorized by tertiles (nonparametric trend z = 3.50, p < 0.001), the relationship between B[a]P and maternal blood adducts was insignificant (z = 1.63, p = 0.103). Based on the multivariable linear regression model we estimated the effect of the prenatal airborne B[a]P on the level of cord blood adducts. In total, 14.8% of cord blood adducts variance was attributed to the level of maternal adducts and 3% to a higher prenatal B[a] exposure above 5.70 ng/m3. The calculated fetal/maternal blood adducts ratio (FMR) linearly increased with the B[a]P exposure (z = 1.99, p = 0.047) and was highest at B[a]P concentrations exceeding 5.70 ng/m3.
In conclusion, the results support other findings that transplacental exposure to B[a[P from maternal inhalation produces DNA damage in the developing fetus. It also confirms the heightened fetal susceptibility to prenatal PAH exposure that should be a matter of public health concern particularly in the highly polluted areas because DNA adducts represent a pro-carcinogenic alteration in DNA The continuation of this birth cohort study will assess the possible health effects of fetal DNA damage on health of children and help in establishing new protective guidelines for newborns.
PMCID: PMC3733112  PMID: 23299301
prenatal exposure; polycyclic aromatic hydrocarbons; biomarkers of exposure; PAH-DNA adducts; birth cohort study
The main goal of the study was to determine the relationship between prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) measured by PAH-DNA adducts in umbilical cord blood and early wheeze. The level of PAH-DNA adducts in the cord blood is assumed to reflect the cumulative dose of PAHs absorbed by the fetus over the prenatal period. The effect of prenatal PAH exposure on respiratory health measured by the incidence rate ratio (IRR) for the number of wheezing days in the subsequent four year follow-up was adjusted for potential confounding factors such as personal prenatal exposure to fine particulate matter (PM2.5), environmental tobacco smoke (ETS), gender of child, maternal characteristics (age, education and atopy), parity, and mold/dampness in the home. The study sample includes 339 newborns of non-smoking mothers 18-35 years of age and free from chronic diseases, who were recruited from ambulatory prenatal clinics in the first or second trimester of pregnancy. The number of wheezing days during the first two years of life was positively associated with prenatal level of PAH-DNA adducts (IRR = 1.69, 95%CI = 1.52 – 1.88), prenatal particulate matter (PM2.5) level dichotomized by the median (IRR = 1.38; 95%CI: 1.25 – 1.51), maternal atopy (IRR = 1.43; 95%CI: 1.29 – 1.58), moldy/damp house (IRR = 1.43; 95%CI: 1.27 – 1.61). The level of maternal education and maternal age at delivery were inversely associated with the IRRs for wheeze. The significant association between frequency of wheeze and the level of prenatal environmental hazards (PAHs and PM2.5) was not observed at ages 3 or 4 years. Although the frequency of wheezing at ages 3 or 4 years was no longer associated with prenatal exposure to PAHs and PM2.5, its occurrence depended on the presence of wheezing in the first two years of life, which nearly tripled the risk of wheezing in later life. In conclusion, the findings may suggest that driving force for early wheezing (<24 months of age) are different to those leading to later onset of wheeze. As we reported no synergistic effects between prenatal PAH (measured by PAH-DNA adducts) and PM2.5 exposures on early wheeze, this suggests the two exposures may exert independent effects via different biological mechanism on wheeze.
PMCID: PMC3683604  PMID: 20444151
prenatal exposure to polycyclic aromatic hydrocarbons; biomarkers of exposure; DNA adducts; early wheeze; 4-year olds; birth cohort study
We previously reported an association between prenatal exposure to airborne PAH and lower birth weight, birth length and head circumference. The main goal of the present analysis was to assess the possible impact of co-exposure to PAH-containing of barbecued meat consumed during pregnancy on birth outcomes.
The birth cohort consisted of 432 pregnant women who gave birth at term (>36 weeks of gestation). Only non-smoking women with singleton pregnancies, 18-35 years of age, and who were free from chronic diseases such as diabetes and hypertension were included in the study. Detailed information on diet over pregnancy was collected through interviews and the measurement of exposure to airborne PAHs was carried out by personal air monitoring during the second trimester of pregnancy. The effect of barbecued meat consumption on birth outcomes (birthweight, length and head circumference at birth) was adjusted in multiple linear regression models for potential confounding factors such as prenatal exposure to airborne PAHs, child’s sex, gestational age, parity, size of mother (maternal prepregnancy weight, weight gain in pregnancy) and prenatal environmental tobacco smoke (ETS).
The multivariable regression model showed a significant deficit in birthweight associated with barbecued meat consumption in pregnancy (coeff = −106.0 g; 95%CI: −293.3, −35.8); The effect of exposure to airborne PAHs was about the same magnitude order (coeff. = −164.6 g; 95%CI: −172.3, − 34.7). Combined effect of both sources of exposure amounted to birth weight deficit of 214.3 g (95%CI: −419.0, − 9.6). Regression models performed for birth length and head circumference showed similar trends but the estimated effects were of borderline significance level. As the intake of barbecued meat did not affect the duration of pregnancy, the reduced birthweight could not have been mediated by shortened gestation period.
In conclusion, the study results provided epidemiologic evidence that prenatal PAH exposure from diet including grilled meat might be hazardous for fetal development.
PMCID: PMC3288524  PMID: 22079395
barbecued meat; pregnancy; birth weight; birth cohort study
6.  Effects of Prenatal and Perinatal Exposure to Fine Air Pollutants and Maternal Fish Consumption on the Occurrence of Infantile Eczema 
As there is a scarcity of evidence on potential hazards and preventive factors for infantile eczema operating in the prenatal period, the main goal of this study was to assess the role of prenatal exposure to fine particulate matter and environmental tobacco smoke (ETS) in the occurrence of infant eczema jointly with the possible modulating effect of maternal fish consumption.
The study sample consisted of 469 women enrolled during pregnancy, who gave birth to term babies (>36 weeks of gestation). Among all pregnant women recruited, personal measurements of fine particulate matter (PM2.5) were performed over 48 h in the second trimester of pregnancy. After delivery, every 3 months in the first year of the newborn's life, a detailed, standardized, face-to-face interview was administered to each mother, in the process of which a trained interviewer recorded any history of infantile eczema and data on potential environmental hazards. The estimated risk of eczema related to higher prenatal exposure to fine particulate matter (PM2.5 >53.0 μg/m3) and postnatal ETS as well as the protective effect of maternal fish intake were adjusted for potential confounders in a multivariable logistic regression model.
While the separate effects of higher prenatal PM2.5 and postnatal ETS exposure were not statistically significant, their joint effect appeared to have a significant influence on the occurrence of infantile eczema [odds ratio 2.39, 95% confidence interval (CI) 1.10–5.18]. With maternal fish intake of more than 205 g/week, the risk of eczema decreased by 43% (odds ratio 0.57, 95% CI 0.35–0.93). The incidence rate ratio (IRR) for eczema symptoms, estimated from the Poisson regression model, was increased with both higher exposure to prenatal PM2.5 and postnatal ETS (IRR 1.55, 95% CI 0.99–2.44) and in children of atopic mothers (IRR 1.35, 95% CI 1.04–1.75) but was lower in girls (IRR 0.78, 95% CI 0.61–1.00). The observed preventive effect of fish consumption on the frequency of eczema symptoms was consistent with the results of the logistic analysis (IRR 0.72, 95% CI 0.52–0.99).
The findings indicate that higher prenatal exposure to fine particulate matter combined with postnatal exposure to ETS may increase the risk of infant eczema, while maternal fish intake during pregnancy may reduce the risk of infantile eczema.
PMCID: PMC3047761  PMID: 21293147
Fish consumption; Prenatal exposure to fine particles; Cow's milk allergy; Passive tobacco smoke; Cohort study
7.  Prohypertensive Effect of Gestational Personal Exposure to Fine Particulate Matter. Prospective Cohort Study in Non-smoking and Non-obese Pregnant Women 
Cardiovascular Toxicology  2012;12(3):216-225.
Exposure to fine particulate matter (PM) is a recognized risk factor for elevated blood pressure (BP) and cardiovascular disease in adults, and this prospective cohort study was undertaken to evaluate whether gestational exposure to PM2.5 has a prohypertensive effect. We measured personal exposure to fine particulate matter (PM2.5) by personal air monitoring in the second trimester of pregnancy among 431 women, and BP values in the third trimester were obtained from medical records of prenatal care clinics. In the general estimating equation model, the effect of PM2.5 on BP was adjusted for relevant covariates such as maternal age, education, parity, gestational weight gain (GWG), prepregnancy BMI, environmental tobacco smoke (ETS), and blood lead level. Systolic blood pressure (SBP) increased in a linear fashion across a dosage of PM2.5 and on average augmented by 6.1 mm Hg (95% CI, 0.6–11.6) with log unit of PM2.5 concentration. Effects of age, maternal education, prepregnancy BMI, blood lead level, and ETS were insignificant. Women with excessive gestational weight gain (>18 kg) had higher mean SBP parameters by 5.5 mmHg (95% CI, 2.7–8.3). In contrast, multiparous women had significantly lower SBP values (coeff. = −4.2 mm Hg; 95% CI, −6.8 to −1.6). Similar analysis performed for diastolic blood pressure (DBP) has demonstrated that PM2.5 also affected DBP parameters (coeff. = 4.1; 95% CI, −0.02 to 8.2), but at the border significance level. DBP values were positively associated with the excessive GWG (coeff. = 2.3; 95% CI, 0.3–4.4) but were inversely related to parity (coeff. = −2.7; 95% CI, −4.6 to −0.73). In the observed cohort, the exposure to fine particulate matter during pregnancy was associated with increased maternal blood pressure.
PMCID: PMC3404286  PMID: 22328329
Blood pressure; Exposure to fine particulate matter; Pregnancy; Gestational weight gain; Prepregnancy ponderal index; Environmental tobacco smoke
8.  Higher Fish Consumption in Pregnancy May Confer Protection against the Harmful Effect of Prenatal Exposure to Fine Particulate Matter 
Annals of Nutrition & Metabolism  2010;56(2):119-126.
The objective of this study was to assess a hypothesized beneficial effect of fish consumption during the last trimester of pregnancy on adverse birth outcomes resulting from prenatal exposure to fine air particulate matter.
The cohort consisted of 481 nonsmoking women with singleton pregnancies, of 18–35 years of age, who gave birth at term. All recruited women were asked about their usual diet over the period of pregnancy. Measurements of particulate matter less than 2.5 μm in size (PM2.5) were carried out by personal air monitoring over 48 h during the second trimester of pregnancy. The effect of PM2.5 and fish intake during gestation on the birth weight of the babies was estimated from multivariable linear regression models, which beside the main independent variables considered a set of potential confounding factors such as the size of the mother (height, prepregnancy weight), maternal education, parity, the gender of the child, gestational age and the season of birth.
The study showed that the adjusted birth weight was significantly lower in newborns whose mothers were exposed to particulate matter greater than 46.3 μg/m3 (β coefficient = −97.02, p = 0.032). Regression analysis stratified by the level of maternal fish consumption (in tertiles) showed that the deficit in birth weight amounted to 133.26 g (p = 0.052) in newborns whose mothers reported low fish intake (<91 g/week). The birth weight deficit in newborns whose mothers reported medium (91–205 g/week) or higher fish intake (>205 g/week) was insignificant. The interaction term between PM2.5 and fish intake levels was also insignificant (β = −107,35, p = 0.215). Neither gestational age nor birth weight correlated with maternal fish consumption.
The results suggest that a higher consumption of fish by women during pregnancy may reduce the risk of adverse effects of prenatal exposure to toxicants and highlight the fact that a full assessment of adverse birth outcomes resulting from prenatal exposure to ambient hazards should consider maternal nutrition during pregnancy.
PMCID: PMC2842166  PMID: 20134157
Air pollutants; Prenatal exposure; Fish consumption; Birth size; Cohort study
Environment international  2009;35(6):877-884.
The main goal of the paper was to assess the pattern of risk factors having an impact on the onset of early wheezing phenotypes in the birth cohort of 468 two-year olds and to investigate the severity of respiratory illness in the two-year olds in relation to both wheezing phenotypes, environmental tobacco smoke (ETS) and personal PM2.5 exposure over pregnancy period (fine particulate matter). The secondary goal of the paper was to assess possible association of early persistent wheezing with the length of the baby at birth. Pregnant women were recruited from ambulatory prenatal clinics in the first and second trimester of pregnancy. Only women 18–35 years of age, who claimed to be non-smokers, with singleton pregnancies, without illicit drug use and HIV infection, free from chronic diseases were eligible for the study. In the statistical analysis of respiratory health of children multinomial logistic regression and zero-inflated Poisson regression models were used. Approximately one third of the children in the study sample experienced wheezing in the first two years of life and in about two third of cases (67%) the symptom developed already in the first year of life. The early wheezing was easily reversible and in about 70% of infants with wheezing the symptom receded in the second year of life. The adjusted relative risk ratio (RRR) of persistent wheezing increased with maternal atopy (RRR = 3.05; 95%CI: 1.30 – 7.15), older siblings (RRR = 3.05; 95%CI: 1.67 – 5.58) and prenatal ETS exposure (RRR= 1.13; 95%CI: 1.04 – 1.23), but was inversely associated with the length of baby at birth (RRR = 0.88; 95%CI: 0.76 – 1.01). The adjusted incidence risk ratios (IRR) of coughing, difficult breathing, runny/stuffy nose and pharyngitis/tonsillitis in wheezers were much higher than that observed among non-wheezers and significantly depended on prenatal PM2.5 exposure, older siblings and maternal atopy. The study shows a clear inverse association between maternal age or maternal education and respiratory illnesses and calls for more research efforts aiming at explanation of factors hidden behind proxy measures of quality of maternal care of babies. The data support the hypothesis that burden of respiratory symptoms in early childhood and possibly in later life may be programmed already in prenatal period when the respiratory system is completing its growth and maturation.
PMCID: PMC2709737  PMID: 19394697
wheezing phenotypes; respiratory symptoms; prenatal and postnatal environmental air quality; birth cohort study
10.  Estimating Individual-Level Exposure to Airborne Polycyclic Aromatic Hydrocarbons throughout the Gestational Period Based on Personal, Indoor, and Outdoor Monitoring 
Environmental Health Perspectives  2008;116(11):1509-1518.
Current 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.
We 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.
The 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.
Considering 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.
PMCID: PMC2592271  PMID: 19057704
coal; long-term personal exposure; polycyclic aromatic hydrocarbons; spatial and temporal variability
11.  Estimated Risk for Altered Fetal Growth Resulting from Exposure to Fine Particles during Pregnancy: An Epidemiologic Prospective Cohort Study in Poland 
Environmental Health Perspectives  2004;112(14):1398-1402.
The purpose of this study was to estimate exposure of pregnant women in Poland to fine particulate matter [≤2.5 μm in diameter (PM2.5)] and to assess its effect on the birth outcomes. The cohort consisted of 362 pregnant women who gave birth between 34 and 43 weeks of gestation. The enrollment included only nonsmoking women with singleton pregnancies, 18–35 years of age, who were free from chronic diseases such as diabetes and hypertension. PM2.5 was measured by personal air monitoring over 48 hr during the second trimester of pregnancy. All assessed birth effects were adjusted in multiple linear regression models for potential confounding factors such as the size of mother (maternal height, prepregnancy weight), parity, sex of child, gestational age, season of birth, and self-reported environmental tobacco smoke (ETS). The regression model explained 35% of the variability in birth weight (β = −200.8, p = 0.03), and both regression coefficients for PM2.5 and birth length (β = −1.44, p = 0.01) and head circumference (HC; β = −0.73, p = 0.02) were significant as well. In all regression models, the effect of ETS was insignificant. Predicted reduction in birth weight at an increase of exposure from 10 to 50 μg/m3 was 140.3 g. The corresponding predicted reduction of birth length would be 1.0 cm, and of HC, 0.5 cm. The study provides new and convincing epidemiologic evidence that high personal exposure to fine particles is associated with adverse effects on the developing fetus. These results indicate the need to reduce ambient fine particulate concentrations. However, further research should establish possible biologic mechanisms explaining the observed relationship.
PMCID: PMC1247567  PMID: 15471732
air pollutants; cohort study; fetal growth; pregnancy; prenatal exposure
12.  Prenatal exposures to phthalates among women in New York City and Krakow, Poland. 
Environmental Health Perspectives  2003;111(14):1719-1722.
Experimental evidence has shown that certain phthalates can disrupt endocrine function and induce reproductive and developmental toxicity. However, few data are available on the extent of human exposure to phthalates during pregnancy. As part of the research being conducted by the Columbia Center for Children's Environmental Health, we have measured levels of phthalates in 48-hr personal air samples collected from parallel cohorts of pregnant women in New York, New York, (n = 30) and in Krakow, Poland (n = 30). Spot urine samples were collected during the same 48-hr period from the New York women (n = 25). The following four phthalates or their metabolites were measured in both personal air and urine: diethyl phthalate (DEP), dibutyl phthalate (DBP), diethylhexyl phthalate (DEHP), and butyl benzyl phthalate (BBzP). All were present in 100% of the air and urine samples. Ranges in personal air samples were as follows: DEP (0.26-7.12 microg/m3), DBP (0.11-14.76 microg/m3), DEHP (0.05-1.08 microg/m3), and BBzP (0.00-0.63 microg/m3). The mean personal air concentrations of DBP, di-isobutyl phthalate, and DEHP are higher in Krakow, whereas the mean personal air concentration of DEP is higher in New York. Statistically significant correlations between personal air and urinary levels were found for DEP and monoethyl phthalate (r = 0.42, p < 0.05), DBP and monobutyl phthalate (r = 0.58, p < 0.01), and BBzP and monobenzyl phthalate (r = 0.65, p < 0.01). These results demonstrate considerable phthalate exposures during pregnancy among women in these two cohorts and indicate that inhalation is an important route of exposure.
PMCID: PMC1241713  PMID: 14594621

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