Environmental exposures associated with abnormal growth include; indoor air pollution from biomass fuel combustion (111
) (questionnaire data); benzene (112
). Exposure to particulates (PM2.5) and NO2 is associated with increased risk for growth restriction (113
) (linked birth certificates with LMP and environmental monitoring data).
A survey of air pollutants (SO2, NO2, O3, CO and PM2.5) and impact on fetal growth was explored in three Canadian cities (Calgary, Edmonton, and Montreal) (114
). Exposure was determined from air monitoring stations and birth data from vital statistics. The data suggested an inverse relationship between exposure to NO2, CO and PM2.5 and fetal growth. A similar study in Brisbane, Australia (115
) measuring fetal growth and NO2, PM10 and O3 did not observe an inverse relationship between these pollutants and proxy measures for fetal growth (head circumference, crown-heel length, and small for gestational age). Differences in air pollutant composition may account for this as NO2 concentrations were higher in Canada and O3 concentrations higher in Brisbane.
Several studies have demonstrated ethnic differences in response to PAH and fetal growth (63
), with growth and gestational length is inversely related to PAH exposure among African-Americans but not Dominicans in New York City. Studies with personal monitoring demonstrated an association with PAH and perinatal growth restriction (116
). While a study in S. Korea supports effects from exposures early in the pregnancy, a study in China finds a relationship only from exposures during the third trimester (118
). Results from North America, where levels of pollution are lower, typically find an association between reduced birth weight and PM, but the findings are variable. Studies in California have found some association with PM, though in southern California not when adjusting for gaseous pollutants (119
). There was no association between PM and low birth weight in a study in the northeastern United States (122
), and a study in Canada found a small, but insignificant association with low levels of PM (123
Collaborators in New York and Poland have contributed much to our understanding of air pollution and developmental disease. Recently they explored the role of prenatal particulate exposure (PM2.5) during pregnancy and growth (124
) using personal exposure monitors. Previous work demonstrated that prenatal exposure to air pollutants is associated with growth impairment at birth (length, weight and head circumference), this work explored sex differences in response to prenatal exposure and growth. As PM2.5 levels increased fetal growth was impaired more in male than female fetus, other studies have suggested that the female was more sensitive to the effect of air pollution on birth weight, while males were more sensitive to effect of air pollution on preterm birth (125
A study by Hansen explored ultrasound characterization of fetal growth in relationship to air pollution (126
); femur length, abdominal circumference, head circumference and biparietal diameter. Air pollution exposures were monthly averages of PM10, SO2, NO2 and O3. This study demonstrates that as distance from the air monitoring station increases, adverse effect on fetal growth diminishes, reinforcing the benefit of personal monitoring and biomarkers of exposure.
Paternal exposures before pregnancy and maternal exposures before and during pregnancy to welding and metal fumes and dusts were associated with adverse pregnancy outcome. Paternal exposures may be associated with premature delivery and maternal exposures with impaired growth and prematurity (60
) (exposures defined by questionnaire data and health outcomes by pregnancy records).
The Danish National Birth Cohort Study (DNBC) has evaluated maternal fatty fish consumption (127
) exposure to PCBs, and fetal and placental growth (128
). They observed that greater ingestion of fatty fish was associated with greater concentrations of PCBs and greater concentrations of PCBs was associated with impaired fetal and placental growth. The DNBC has also explored the association between the persistent organic pollutants perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) on fetal and placental growth (129
) demonstrating an inverse association between PFOA and fetal growth.
Drinking water may contain diverse array of pollutants including products resulting from disinfection treatment. Studies using infrequent ecological exposure assessment have suggested adverse developmental consequences. A study collected water samples every week from the distribution system utilized by the subjects, and was unable to discern a relationship between drinking water exposures and developmental outcomes (130