Moms and POPs: birth defects linked to banned, current pollutants.
Ren, A, Q Xinghua, L Jin, J Ma, Z Li, L Zhang, H Zhu, RH Finnell and T Zhu. 2011. Association of selected persistent organic pollutants in the placenta with risk of neural tube defects. Proceedings of the National Academy of the Sciences http:dx.doi.org/10.1073/pnas.1105209108.
The research reveals a complicated picture in which some POPs are cultprits while others are not. For some, the higher the levels measured the higher the risk for the neural tube birth defects. Other pollutants had no associations with the birth defects.
This study is the first to directly link placental levels of multiple POPs to neural tube defects. The results strongly suggest that lingering environmental factors continue to damage fetal development and health.
Multiple chemicals were measured in each woman, and some of them – PAHs and DDT – were found in more than 80 percent of the participants. The PAHs, which are released when fossil fuels burn, and banned legacy pollutants such as the pesticide DDT were associated with neural tube damage.
During fetal development, the neural tube becomes the brain and spinal cord. Serious birth defects like anencephaly and spina bifida arise when the neural tube fails to seal during development. The result is that fetuses can spontaneously abort, and babies can be stillborn or develop lifelong health problems.
Every year, neural tube defects affect more than 300,000 babies worldwide (March of Dimes Foundation 2006). In 2006, the rate of anencephaly in the United States was 12 per every 1,000 live births. In the same year, 18 of every 1,000 babies were born with spina bifida (Martin et al. 2006).
Persistent organic pollutants (POPs) are a broad class of environmentally-prevalent chemicals. They include types of pesticides and flame retardants and are components or byproducts of fossil fuel burning and extraction. The wide collection of POPs compounds are chemically stable, so they stick around in the environment – or persist – for long periods of time. Their levels can increasingly magnify – or bioaccumulate – in animals the higher they are on the food chain. They congregate mostly in fats.
POPs are toxic to humans and wildlife. Exposure to certain types are associated with reproductive, endocrine and immune system effects. Some – like polycyclic aromatic hydrocarbons (PAHs) that are released from gas and coal combustion – are suspected carcinogens. Under the Stockholm Convention, a number of POPs were banned from use, including many examined in this study.
In humans, pesticide POPs exposure in field workers, residents of agricultural communities or home and garden pesticide users have been linked with elevated risks of neural tube defects (Brender et al. 2010; Lacasaña et al. 2006; Rull et al. 2006). In one U.S. study, women whose homes were professionally sprayed for pests were 60 percent more likely to carry a baby with a neural tube defect (Shaw et al. 1999). The pesticide exposure in these studies was self-reported so differences in exposure levels were estimated, not measured. Also, these studies generally looked at a single pesticide when, in reality, moms were likely exposed to a complex mixture of POPs.
A recent study that directly measured PAH levels in mothers’ blood found that increased blood levels were related to neural tube defects in babies (Naufal et al. 2010).
Researchers looked for an association between levels of POPs in the placenta of Chinese women who had just given birth and neural tube defects in their children.
Researchers examined 80 cases of fetuses or newborns with neural tube defects and 50 healthy controls from rural counties in the Shanxi Province in the People’s Republic of China. This province has the highest PAH emissions in the country. The pollutants in question are produced mainly from mining and burning coal. The Shanxi province also has the highest rates of neural tube defects in China at 14 per every 1,000 births.
At birth, the scientists measured several types of POPs in placental tissue, including 10 types of PAHs and multiple types of organochloride pesticides: lindane (gamma-HCH) and two byproducts of alpha-HCH and beta-HCH, HCB and alpha-endosulfan. They also measured two types of the pesticide DDT and a number of DTT metabolites – the common chemicals produced when the body breaks down DTT.
Measuring levels of chemicals in the placenta is commonly used to approximate fetal exposure to chemicals.
Investigators reported that some – but not all – POPs were associated with a higher risk for carrying a baby with a defect. The strongest association was found with PAHs, chemicals that were detected in 82 to 100 percent of mothers-to-be.
Researchers found that moms that carried a baby with a neural tube defect were nearly five times as likely to have elevated levels of up to 10 different PAHs in their placentas. What’s more, the higher the level of placental PAHs, the larger the risk.
DDT and HCH pesticides were banned in China in 1983. Yet, every type of DDT and HCH measured for was detected in most of the placental tissues sampled – 78 to 100 percent depending on the chemical.
In contrast to PAHs, only some of the DDT or HCH chemicals were associated with neural tube defects. In particular, moms were three times as likely to carry a fetus with a neural tube defect if they had higher levels of alpha-HCH, but not beta-HCH or gamma-HCH. Similarly, only a particular type of DDT called o,p’-DDT or its metabolites, was associated with elevated risk for neural tube defects.
For the chemicals that were linked to neural tube defects, the larger the placental levels, the more likely the babies were to harbor neural tube defects.
Not all POPs examined were linked to increased risk for neural tube defects. For example, higher levels of p,p’-DDT, beta-HCH, gamma-HCH or the fungicide hexachlorobenze were not linked to increased risk for neural tube defects.
Specific long-lasting pesticides and currently-released industrial pollutants measured in the placenta of pregnant women are associated with neural tube defects in the infants. The results agree with earlier studies that report a link between neural tube defects and prebirth exposure to numerous types of POPs and PAHs.
This study is unique because researchers directly measured levels of POPs in the placenta as a way to capture a snapshot of fetal exposure to these environmental chemicals.
The scientists found that chemicals still released – like PAHs – and some banned from use for decades – like DTT and HCH – may damage the neural tube during development.
This study was also the first to look at whether higher levels of the chemicals were associated with increasing risk – called a dose-response relationship. With a number of the POPs analyzed, the higher the exposure, the higher the risk of the defects. Combined levels of PAHs showed this pattern.
The exposure levels in this population of Chinese women are high due to nearby coal mining and use. Even so, the results highlight the need to understand links between current exposures and health as well as the lasting risks from legacy pollutants.
Lacasaña, M, H Vázquez-Grameix, VH Borja-Aburto, J Blanco-Muñoz, I Romieu, C Aguilar-Garduño and AM García. 2006. Maternal and paternal occupational exposure to agricultural work and the risk of anencephaly. Occupational and Environmental Medicine 63(10):649-56.
March of Dimes Foundation. 2006. Global Report on Birth Defects: The Hidden Toll of Dying and Disabled Children. http://www.marchofdimes.com/aboutus/15796_18678.asp.
Martin, JA, BE Hamilton, PD Sutton, SJ Ventura, F Menacker, S Kirmeyer and TJ Matthews. 2006. Births: Final Data for 2006. National Vital Statistics Reports, Volume 57, Number 7 (PDF).
Naufal, Z, L Zhiwen, L Zhu, GD Zhou, T McDonald, LY He, L Mitchell, A Ren, H Zhu, R Finnell and KC Donnelly. 2010. Biomarkers of exposure to combustion by-products in a human population in Shanxi, China. Journal of Exposure Science and Environmental Epidemiology 20(4):310-9.
Sever, LE. 1995. Looking for causes of neural tube defects: where does the environment fit in? Environmental Health Perspective 103(Suppl 6):165–171.
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Polycyclic aromatic hydrocarbons