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Chlorinated water and pregnancy – how it affects fetal development and why genes matter

pregnant woman holding stomach

If you’re interested in making your water safer for you and your family, you probably saw this study which found unsafe levels of many carcinogens in United States drinking water. The study was picked up by USA Today and many national news outlets.

It’s against that backdrop that we delve into the issue of chlorine in water and how it can affect prenatal health. This is a bit of a nerdy post, so if you have questions, please submit them here for inclusion on a future podcast episode.

If you’re pregnant or trying to conceive, you probably already know that the mix of genes in egg and sperm play a role in determining things like your baby’s eye color and whether they have curly or straight hair. What you might not know is that parental genes also affect the impact on your baby of chemicals the birth parent is exposed to during pregnancy. In recent years, researchers have published several studies that suggest our genes affect the impact of prenatal exposure to chemicals. Indeed, one study has now found that people with certain genetic variants are more susceptible to chlorination by-products in drinking water, leading to a greater risk of having a small-for-gestational age baby.

Previous studies have also noted an association between CBP exposure and reduced fetal growth, but these studies didn’t go as far as investigating a potential mechanism behind this association. This study is one of the first to look specifically at how a person’s genome may increase susceptibility to contaminants in treated drinking water.

Before we dig into the latest research, here’s a quick overview of why many of us are exposed to chlorination by-products in the first place.

Chlorination of drinking water

Chlorine has long been widely used as a disinfectant for drinking water. The adoption of chlorine as a disinfectant for drinking water was one of the most significant developments in public health in the last century. Without a doubt, chlorine disinfection has helped save millions of lives that may otherwise have been lost to pathogenic infection with Escherichia coli, Cryptosporidium, and other microorganisms. The benefits of chlorine disinfection are inarguable, but that doesn’t mean chlorine treatment is completely safe.

Concern has grown in recent years over the potential adverse health effects of disinfectant byproducts (DBPs), and a new study suggests that certain genetic polymorphisms may increase the likelihood of impaired infant development in those exposed to DBPs during pregnancy.

Why might this happen? To understand that, we need to understand some basics about chlorine and what happens when we use it to disinfect drinking water.

Chlorine is a very reactive gas that interacts with natural organic matter in water to kill undesirable microorganisms. Unfortunately, chlorine and other disinfectants also react with organic matter and bromine to form more than 600 known disinfectant byproducts (DBPs).

When added to water as either chlorine gas or liquid chlorine bleach, chlorine reacts to form hypochlorous acid and, if bromine is present, hypobromous acid. These acids are both strong oxidizing agents and very reactive, which is precisely why they’re effective disinfectants. In 1974, however, Rook discovered that these two acids also react with organic matter in water to create disinfection by-products. These include the four primary trihalomethanes: chloroform, bromodichloromethane, dibromochloromethane, and bromoform. 1

Around 80 haloacetic acids (HAAs) and trihalomethanes (THMs), including chloroform, bromodichloromethane (BDCM), dibromochloromethane (DBCM), and bromoform, have been found in drinking water in the US. 2 These were identified in the 1950s and are the most prevalent chlorinated by-products (CBPs) and the most abundant DBPs identified. 3

The trihalomethanes (THMs) are so called because they consist of a carbon atom surrounded by and bound to four atoms comprising one hydrogen and three halogens, namely chlorine and bromine. THMs and HAAs tend to be used as an indication of the presence of all potentially harmful chemicals formed when chlorine is added to water. Regulations rely to a great extent on this model to control exposure to all DBPs.

Drinking water is not the only source of DBP exposure, though. As well as oral exposure, DBPs may make their way into the body through dermal contact or inhalation. Indeed, hot showers and baths may be the most significant source of exposure in many people. 4 Those who regularly swim in chlorinated pools may also have a high level of exposure to DBP through inhalation and dermal contact.5

In the US, the frustrating situation persists where DBCM and bromoform are not classified as potential carcinogens like chloroform and BDCM. Neither are they classed as non-carcinogenic, however. There’s simply not enough information either way, and so they remain present to some degree in the water supply.

THMs have been regulated since 1979, based on their association with an increased risk of developing cancer. 6 Specifically, long-term chronic DBP exposure from drinking water was associated with an increased likelihood of bladder, colorectal, and liver cancer. 78910 In 1998, regulators turned their attention to haloacetic acids (HAAs) which were also found to occur frequently in the disinfected water supply. 11

The US Environmental Protection Agency only sets standards for total THMs, not for individual chemicals. In other countries, particularly those in Europe, much stricter standards exist for DBPs in drinking water. This is based on the precautionary principle, which is the idea that we do best by avoiding chemicals until they are proven safe.

So, how do European countries and others keep drinking water safe while keeping DBP levels low? By using ultraviolet light, ozone, chloramines and other water treatment and filtration strategies, that’s how.

In the US, community water suppliers are required to carry out regular tests on finished drinking water to ensure DBP levels are below established standards. Unfortunately, testing methods may not be as robust as previously thought, with a 2017 study finding that long-term annual compliance (LRAA) or quarterly (QA) data did not accurately reflect short-term exposure to DBPs. 12

This paper, published in the International journal of environmental research and public health, looked at ways to measure DBPs in drinking water in the US. Because there’s a lack of short-term data on DBPs, the researchers looked at the usefulness of the long-term measurements typically used by epidemiologists to assess exposure levels, i.e. the LRAA or QA data. They found that this data might not be as useful as previously thought for assessing risk. What’s more, this discrepancy might go some way towards explaining why research has so far been inconclusive when looking at the association between DBP exposure and adverse birth outcomes. After all, risk assessors are only as good as their data.

What does the science say about chlorination by-products?

Acknowledging the potential adverse effects of these chemicals, the World Health Organization (WHO) created guidelines for acceptable levels of CBPs (and DBPs in general) in drinking water. These guidelines, as with so many others concerning chemical exposure, are based on research involving non-human animals, including beagles, rats, and mice. One study looked at dogs over 7.5 years, but others were very short-term, lasting just 90 days.

In recent years, researchers have focused more on the health effects of DBPs in humans. Studies have looked at the long-term health outcomes linked to exposure to DBPs in drinking water and in water used for bathing, showering, and elsewhere in the home. Results from these studies should give us pause when designing new systems for treating drinking water, especially now we have other technologies available to decontaminate water.

Don’t misunderstand me, disinfection of water is vital to support public health. The WHO stresses that waterborne pathogens are far more likely to cause health issues, especially immediate health effects, than DBPs are. As such, disinfection of water should never be compromised in trying to meet DBP guidelines; “water disinfection by-products are certainly the lesser of these two evils”.

However, we should also continue to improve our awareness of the potential negative effects of chlorination and find ways to minimize risks overall. It’s also notable that some SNPs have been linked to an increased risk of adverse effects from lead, which is another potential contaminant in drinking water. 13

So, what about this latest study addressing prenatal exposure to chlorination by-products?

Impaired fetal development, genes, and drinking water contaminants

In this more recent study, researchers set out to assess the effects of maternal exposure to DBPs on fetal development. Specifically, they looked at babies who were small for their gestational age (SGA). This means that, regardless of whether a baby was born at full-term or prematurely, their weight was below the 10th percentile (i.e. 90% of other infants would weigh more) for that week of pregnancy.

The case-control study matched 1432 mother-child pairs and looked to see if specific single nucleotide polymorphisms (SNPs) in genes coding for CYP450 enzymes were associated with SGA infants. They also looked at the interaction between these SNPs and maternal exposure to CBPs during the final (third) trimester of pregnancy.

Their conclusion?

There is some evidence that CBPs affect fetal growth, and your genes may influence how much of an effect CBPs have during pregnancy.

As for the specifics, the researchers looked at SNPs within CYP1A2, CYP2A6, CYP2D6 and CYP17A1 genes. The latter gene seems to be the one with the most significant potential for interaction with exposure to CBPs. The other genetic variants, in CYP1A2, CYP2A6, and CYP2D6, did not remain statistically significant (i.e. were likely to be down to chance) after correction for multiple testing. These results are similar to an earlier European study that also didn’t find an association between SNPs in these genes and the risk of SGA. 14

However, although the evidence is weak, it seems that CBP exposure may restrict fetal growth more profoundly where newborns carry CYP17A1 rs4919687 A and rs743572 G alleles.

The researchers found that the likelihood of a baby being significantly smaller than average was around 10-30% higher if the child carried CYP17A1 rs4919687 A and rs743572 G alleles and the birth parent was exposed to higher levels of TTHMs and HAAs.

In contrast, TTHMs exposure in mothers with CYP17A1 rs4919687 A and rs743572 G alleles was associated with a lower likelihood of having an SGA infant. The effect of neither the newborn nor maternal SNPs remained statistically significant after correcting for multiple testing, but the results do suggest that the CYP17A1 gene may modulate the impact of maternal chemical exposure.

So, why might the CYP17A1 gene, and the enzymes produced thanks to this gene, affect fetal development in response to CBP exposure in pregnancy?

CYP enzymes and SGA

The 1-3 family of CYP enzymes are responsible for oxidative reactions in the metabolism of xenobiotics, i.e. chemicals entering the body rather than produced by the body. Some of these enzymes play a role in bioactivating xenobiotics, potentially transforming harmless chemicals into metabolites that are reactive and damaging. 15

CYP2E1 is the primary enzyme involved in chloroform metabolism, for instance, leading to free radical production and electrophilic phosgene which cause oxidative stress. 161718 Oxidative stress in pregnancy has been linked to impaired fetal development and abnormal fetal growth. 192021

Human isoenzymes CYP1A2 and CYP2A6 metabolize bromodichloromethane (BDCM), one of the four primary THMs. 2223


The isoenzyme CYP17A1 plays a role in the synthesis of sex steroid hormones in the placenta, adrenal glands and gonads. 2425 CYP17A1 mediates the activity and function of two key enzymes involved in human sex steroid hormone production: 17α-hydroxylase and 17,20-lyase. 26 Alterations in the function of this gene and the resulting enzyme may, therefore, affect fetal growth.

Two other case-control studies have already noted an interaction between CYP17A1 polymorphisms and the risk of fetal growth being affected by environmental chemical exposure. 27 In these cases, maternal CYP17A1 genotype A1A1 and prenatal alcohol consumption or cord blood levels of endosulfan, an organochlorine pesticide, were associated with reduced birth weight. 28

To examine this interaction more closely, we might consider the CYP17A1 A2 (rs743572 G) allele. This allele is thought by some to increase the synthesis of precursor androgens and their conversion to estrogens, leading to an increased rate of transcription. 29 As estrogens stimulate the function of the placenta and cellular proliferation, they play a key role in fetal growth. 30

An earlier study found that women who were homozygous for CYP17A1 A1 (rs743572 A) were more than three times as likely to have an SGA infant than mothers carrying the allele CYP17A1 A2 (rs743572 G). 31

One key thing to note in this study is that the researchers did not find a statistically significant risk between maternal genotype alone and the likelihood of SGA and interaction with CBPs. Previous studies have focused, seemingly exclusively, on maternal genotype, introducing the potential for confounding due to the infants’ genotypes potentially being different. Put more simply, a baby inherits genetic material from both biological parents, so their specific genotype is not an exact match for either biological parent.

Interestingly, another study found an association between the homozygous genotype for CYP17A1 rs4919687 A allele and coronary artery disease; 32 maternal cardiovascular issues, such as preeclampsia, have been associated with SGA. 33 Other researchers have noted that CBPs are potential endocrine disruptors, and that higher levels of exposure to THMs could decrease total testosterone levels, resulting in androgenic deficiency and impaired growth. 343536

The takeaway – what does this mean for you?

There’s a lot more information out there on the activity of CYP17A1, for now, though, it seems that this gene may well affect the impact of endocrine-disrupting chemicals in pregnancy, affecting fetal development.

As such, if you’re thinking about conceiving or are already pregnant, you might want to check your genotype and that of the other biological parent. Your results should show whether you carry the CYP17A1 polymorphism or any others linked to altered metabolism of potential toxicants. In one study, genetic variants in the CYP2D6 were a significant predictor of baseline blood concentrations of THMs and concentrations 10 and 30 minutes after showering.37

If both biological parents are tested, this offers a decent indication as to the likely genotype of your offspring, i.e. which alleles they’re likely to inherit.

This could help you prioritize lifestyle changes to support a healthy pregnancy. This might mean:

  • Contacting your local water authority for information on chlorination by-product levels
  • Sending your tap water for testing yourself
  • Installing a water filtration and purification system in your home if levels of CBPs or total DBPs are higher than you’d like.

Remember, though, even if you don’t have the SNP in question, your baby might, and you won’t know that until they’re born. As such, if you have any concerns about chlorine by-products in your household water supply, consider installing either a whole home water filtration system, or a countertop water filter. And don’t forget to filter your shower or bath water! Some people get more exposure to CBPs and DBPs in general from water they don’t drink.

Leigh Matthews, BA Hons, H.Dip. NT

Leigh Matthews, BA Hons, H.Dip. NT, is a health and wellness writer for Gene Food specializing in plant-based nutrition. Read her full bio here.

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