Serial urinary BPA concentrations were highly variable, had a low degree of reproducibility, and varied according to time of day of sample collection in the latter two-thirds of pregnancy. Occupational, dietary, and environmental factors were associated with urinary BPA concentrations. Working as a cashier, canned vegetables consumption, tobacco smoke exposure, and exposure to high-molecular-weight phthalates were positively associated with urinary BPA concentrations. Differences in prenatal urinary BPA concentrations among categories of some of these factors were of similar magnitude to differences in prenatal urinary BPA concentrations associated with externalizing behaviors in 2-year-old females in a prior study (Braun et al. 2009
Our reported ICC (0.11) for repeated urinary BPA concentrations is lower than previous reports. Nepomnaschy et al. (2009)
reported an ICC of 0.43 for three urinary BPA concentrations taken at 14-day intervals from 60 women of childbearing age. Teitelbaum et al. (2008)
reported ICCs of 0.22–0.35 for urinary BPA concentrations among children 6–10 years of age over a 6-month period. Consistent with our findings, Adibi et al. (2008)
reported a decreased ICC of urinary concentrations of phthalate metabolites in pregnant women when they adjusted for urine dilution using creatinine. Variations in the ICCs across studies could be related to differences in time between urine collections or increased creatinine excretion during pregnancy (Williams 2005
Among demographic and perinatal factors, only maternal education was inversely associated with creatinine-standardized urinary BPA concentrations during pregnancy. A study using data from the National Health and Nutrition Examination Survey reported that income was inversely associated with urinary BPA concentrations (Calafat et al. 2008
). However, two studies from China and the Netherlands documented higher urinary BPA concentrations among persons from higher social class (He et al. 2009
; Ye et al. 2008
). Women from lower social classes in the United States may consume more canned foods or live in neighborhoods where more canned fruits and vegetables are available than do women with higher socioeconomic status, but these relationships may be different in other countries (Morland and Filomena 2007
). Furthermore, associations between urinary BPA concentrations and maternal education may be influenced by shared covariance with occupation or tobacco smoke exposure.
The frequency of consumption of canned vegetables, but not canned fruit, was positively associated with urinary BPA concentrations. We are not aware of any prior studies documenting this association, but this finding is not surprising because BPA can migrate from consumer goods into food and has been detected in canned foods (Cao et al. 2010
; Kang and Kondo 2002
; Thomson and Grounds 2005
). A recent risk assessment suggests that canned vegetables contribute 10–40% of the daily BPA intake, whereas canned fruits contribute 3–6% (von Goetz et al. 2010
). The relative contribution of canned vegetables to total BPA dose may vary according to the canning process, food variety, type of resin used, and, as shown here, frequency of consumption. Dietary patterns such as vegetarianism may influence BPA exposure, as suggested by the different concentrations among strict, partial, and nonvegetarians. However, we had a small number of women following a vegetarian diet, and the higher exposure among partial vegetarians is inconsistent with the lower concentration among strict vegetarians.
Compared with other occupations, cashiers had the highest urinary BPA concentrations. Most carbonless paper receipts used in convenience and grocery stores contain BPA, which could be dermally absorbed, orally ingested, or inhaled (vom Saal and Myers 2008
). These results should be interpreted cautiously because estimates from cashiers were based on 17 women and were attenuated with adjustment for socioeconomic factors. Additional studies should validate our findings and, if they are validated, determine the primary route of exposure and if personal protective equipment (e.g., gloves) could prevent exposure.
Two common environmental exposures, phthalates and tobacco smoke, were positively associated with urinary BPA concentrations. Women with secondhand or active tobacco smoke exposure had urinary BPA concentrations about 20% higher than women with no tobacco smoke exposure. This finding is consistent with a prior study reporting higher urinary BPA concentrations among self-reported smokers (He et al. 2009
). Inhaled and exhaled tobacco smoke may be a source of BPA because BPA comprises 25% of the weight of some cigarette filters (Jackson and Darnell 1985
). Although socioeconomic factors may be partly responsible for the association between serum cotinine and urinary BPA concentrations, our estimates were not attenuated after adjustment for socioeconomic factors. Shared sources of BPA and high-molecular-weight phthalates, including DEHP, may be responsible for the positive correlation between urinary BPA and phthalate metabolite concentrations. These phthalates and BPA may be used in the same products (e.g., food packaging), whereas low-molecular-weight phthalates are used in cosmetics and beauty products (NRC 2008
). Future studies should examine other potential sources of BPA and phthalate exposure.
These results have several implications for etiological studies of prenatal BPA exposure and health outcomes. Because urinary BPA concentrations varied according to the time of sample collection and fasting time, investigators should attempt to account for the inherent variability of urinary BPA concentrations. Future studies could use several approaches to reduce or adjust for this variability: a) standardize the timing of urine collection, b) collect multiple urine samples over the course of ≥ 1 days, or c) record and adjust for the time of day of sample collection. The low ICC for urinary BPA concentrations during pregnancy suggests that a single spot urine collection has the potential to misclassify exposure. Moreover, using mean BPA concentrations taken over the course of pregnancy may also result in exposure misclassification in studies attempting to identify time-sensitive windows of development to BPA exposure.
Studies examining the health impacts of prenatal BPA, phthalates, or tobacco smoke exposures may need to adjust for one another, because these pollutants frequency occur together and have been implicated in the etiology of childhood health outcomes (DiFranza et al. 2004
; Engel et al. 2010
; Wakschlag et al. 2002
). In addition, future etiological studies should examine the joint effects of BPA, phthalates, and tobacco smoke exposure, because these common toxicants may occur together and act synergistically on certain health outcomes.
There are several limitations to this study. First, our results and others demonstrate that a single spot urine measurement has the potential to misclassify BPA exposure (Mahalingaiah et al. 2008
). Second, many of our predictor variables were measured imperfectly, and we were missing some potentially important sources of exposure. We did not have women’s occupations classified by an industrial hygienist, which likely resulted in misclassification of this variable. Furthermore, the dietary variables used in this study were not originally designed to assess BPA exposure, but rather pesticide and mercury exposure. In addition, urinary BPA concentrations likely reflect exposure over the last day, whereas dietary questionnaire data reflected consumption over a longer time (weeks). Third, we did not collect information regarding other potential sources of BPA exposure including plastic or paper/cardboard use, packaged food consumption, medical devices, medications, dental treatment, or amount and type (tap, bottled, or well) of water consumed during pregnancy (Carwile et al. 2009
; Gehring et al. 2004
An additional limitation is the imperfect correction for urine dilution using urinary creatinine concentrations. Pregnancy-induced changes in creatinine metabolism and excretion may occur independently of BPA metabolism and excretion, so the degree of correction of urine dilution may change throughout pregnancy. Our results suggest that creatinine concentrations become progressively lower and more variable throughout pregnancy. Other measures of urine dilution, such as specific gravity, have been used and should be compared with creatinine patterns in pregnancy in future studies (Mahalingaiah et al. 2008
A single spot urine sample may misclassify BPA exposure because of variability of urinary BPA concentrations over the course of pregnancy and day. Future studies should standardize or adjust for the timing of urine collection or measure BPA at multiple times to minimize biases due to within-day and within-woman variability of urinary BPA and creatinine concentrations. Our data suggest that there are numerous and potentially modifiable sources of environmental BPA exposure related to canned vegetable consumption, occupation, and other environmental exposures. Additional research is needed to confirm these findings and determine what other environmental sources contribute to human BPA exposure.