Until now, there have been no studies of effects of personal exposure to fine particles on reproductive health and birth outcomes. Our study draws attention to the fact that not only lower birth weight but also reduction in length and HC at birth might be caused by prenatal exposure to pollutants during pregnancy.
Analysis of personal air samples from the pregnant women enrolled in the Krakow study showed that total personal PM2.5
exposures averaged 43.1 μg/m3
with a range of 10.3–147.3 μg/m. None of the women under study in Krakow reported heavy exposure to dusty environments in the working hours. The PM2.5
level in the Krakow study was very high and had a wide range of exposure, compared with data from the United States, where the range of annual mean for PM2.5
measured in various sites is 1.2–14.2 μg/m3
(U.S. EPA 2003
). However, the PM2.5
exposure observed in Krakow would be comparable with that observed in the Czech Republic, where the daily mean is 35.6 μg/m3
(Dejmek et al. 1999
The analysis of birth outcomes indicated a significant inverse correlation between concentrations of fine particles and fetal growth. The adjusted effect of exposure to PM2.5 was reflected in significantly lower mean weight and length at birth and lower mean HC of newborns. The newborns of mothers exposed to higher concentrations of fine particles (above the median of 36.3 μg/m3) showed shorter length at birth by 0.9 cm. The corresponding reductions in HC and birth weight were 0.3 cm and 128.3 g. We estimated from the regression equations that an increase of exposure from 10 to 50 μg/m3 of fine particles would reduce length at birth by 1.0 cm. The corresponding reductions of HC and birth weight would be 0.5 cm and 140.3 g, respectively.
Our study showed a significant positive interrelationship between self-reported ETS level and total personal exposure to PM2.5, which to a great extent depended on the number of reported cigarettes smoked daily at home. This interrelationship creates difficulties in separating the effect of ETS on the birth outcomes from that attributed to fine particles. However, none of the models with both ETS and PM2.5 showed a significant effect of ETS. Moreover, stepwise regression indicated that adding the ETS variable into the model did not explain better the amount of variability in birth outcomes due to air contamination. Therefore, we think that the effect of ETS confirmed in many previous studies may result from its interrelationship with PM2.5. In studies where the birth outcomes were not controlled by the PM2.5 level, the effect of ETS could be demonstrated.
The biologic mechanisms whereby PM2.5
might cause adverse pregnancy outcomes are unclear. PM2.5
might be a proxy measure of a whole complex of toxic agents present in the environment—including PAHs—that could adversely affect fetal growth. It is well known that fine particles are virtually always present in particle-generating processes, especially combustion processes that generate other toxic agents as well. Typically, the ambient fine particle fraction contains constituents of tobacco and wood smoke, organic compounds, sulfates, metals, and soot (Spengler et al. 2001
). Therefore, it would be reasonable to assume that PM2.5
represents a wide spectrum of environmental hazards that may be implicated in intrauterine fetal growth. Air pollutants may affect DNA, as evidenced by observations that placental DNA adducts are more common in areas with higher levels of pollution (Topinka et al. 1997
) and that altered fetal growth has been associated with PAH–DNA adducts (Perera et al. 1998
Our data indicating that personal exposure to fine particles has a stronger relationship with birth outcomes than does ETS may result from the fact that the measurement of ETS exposure based on interviews with pregnant women could be biased. If respondents underestimated their ETS exposure, then its effect may appear much weaker in comparison with the objective measurements of fine particles. However, the level of fine particles is the function not only of ETS, which is the major source of indoor pollution, but also of PM generated from other sources such as fossil fuel combustion.
Another potential limitation of our study comes from the fact that personal monitoring of exposure to fine particles among pregnant women was performed over the short period of 48 hr in the second trimester of pregnancy. However, to evaluate the correlation between the level of PM2.5 measured over 48 hr in the second trimester of pregnancy with those in the second and the third trimesters, a series of repeated measurements in each trimester was carried out in the subsample of 51 pregnant women who were recruited in the first trimester. The concentration of PM2.5 (mean ± SD) in the second trimester was 44.4 ± 46.5 μg/m3, but it was not significantly different from the mean concentration in the first trimester (46.2 ± 34.0 μg/m3) or in the third trimester (35.9 ± 35.3 μg/m3). The latter results suggest that the mean levels of fine particles were rather stable over the whole pregnancy. This provides some confidence that the measurements of personal level of exposure to fine particles taken in the second trimester may also be representative for other pregnancy periods.
We could also demonstrate that total personal exposure to PM2.5 measured over 48 hr correlated well with the PM10 concentrations obtained from the monitors of the municipal air pollution network of Krakow, which were located in the residence areas of the subjects under study (). We observed consistency between monthly means of PM10 measured by the local ambient monitors and the monthly means of total personal exposure to fine particles measured over 48 hr in the second trimester. This suggests that the extrapolation of ambient measurements to personal exposure may be reasonably approximated. However, the extent to which the ambient measurements reflect the individual exposure level may be different in various populations. First, it would depend largely on the quality of the ambient network of air pollution stations and its appropriate coverage of the given residency areas. Besides different lifestyles and mobility of women over the study period, substantial seasonal changes in air pollution due to weather and meteorologic conditions may be significant.
Correlation between mean monthly personal PM2.5 measurements and mean monthly PM10 concentrations from areawide ambient monitoring (circles). Solid line, regression; dashed lines, 95% CI.
In our study, the most important confounders of the birth outcomes such as the presence of chronic diseases or active tobacco smoking by mothers in pregnancy have been removed through entry criteria. Other risk factors thought to affect the probability of delivery of newborns with lower growth, such as maternal height or prepregnancy weight, gestation age, sex of child, and season of birth, were also accounted for in the analysis.
Over the last decades there has been growing concern over the health effects associated with air pollution. The studies were concerned mainly with morbidity and mortality from respiratory diseases, occurrence of respiratory symptoms, pulmonary function, and physician office visits. To date, there have been a limited number of studies investigating the association between air pollution and adverse birth outcomes, and the conclusions were somewhat inconsistent. A study conducted in China suggested that exposure to TSP and SO2
was associated with an excess risk of preterm delivery (Xu et al. 1995
; Yang et al. 2002
) and LBW (Wang et al. 1997
). Several studies observed an association of TSP and SO2
with LBW and found increased risk of IUGR in a highly polluted region in the Czech Republic (Bobak and Leon 1999
; Dejmek et al. 1999
; Sram 1999
). Ritz and Yu (1999)
found that high concentrations of CO and PM10
during the last trimester of pregnancy may increase the risk of LBW for term babies. Our prior study also showed that, after controlling for dietary and smoking sources of the pollutants, PAH–DNA adducts in cord blood were inversely associated with birth weight, length, and HC (Perera et al. 1998
). In contrast, in a study performed in southern Sweden, Landgren (1996)
could not confirm the hypothesis that air pollution affected the incidence of short gestation and LBW. Some researchers (Bhopal et al. 1994
; Smrcka and Leznarova 1998
) found no association between either residential proximity to a coking plant or major steel and petrochemical industries and birth outcomes in the United Kingdom. The study period, size of the population, and number of cases were large. However, Axelsson and Molin (1988)
found that the miscarriage rate was slightly elevated in areas exposed to emissions from petrochemical industries. None of the studies used personal monitors of PM2.5
in the assessment of exposure.
The results of our study are of public concern because adverse birth outcomes have been associated in other studies with more health problems and reduced cognitive development in childhood (Perera et al. 2002
). Follow-up of the cohort will permit determination of the longer-term sequels of prenatal exposures and adverse birth outcomes. The results of our study may have implications not only for the health and development of children but also for adult health. Epidemiologic studies in children indicate that prenatal hazards that restrict fetal growth may be associated with small but measurable delays in motor and social development through childhood and reduced cognitive development (Bacharach and Baumeister 1998
; Hack et al. 1991
; Hediger et al. 2002
; Saigal 2000
). There is also evidence of associations between birth size and future development of adult diseases, such as type 2 diabetes and coronary artery disease (Godfrey and Barker 2001
; Phillips 2000
). It is believed that these associations arise as a result of the phenomenon of “programming,” which involves persisting changes in structure and function caused by environmental factors during critical and vulnerable periods of early development. However, other explanations, including the operation of genetic factors and programming of certain endocrine axes, have also been suggested to explain this observation.
Our study provides convincing epidemiologic evidence based on a cohort that prenatal exposure resulting from high personal maternal 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 help establish possible biologic mechanisms explaining the observed relationship.