Disinfection Byproducts (DBPs) and Health Effects in Drinking Water

Introduction: The Double-Edged Sword of Disinfection

Drinking water disinfection has dramatically reduced waterborne diseases globally, saving countless lives. However, the chemical processes involved can inadvertently create a new set of challenges: Disinfection Byproducts (DBPs). These compounds form when disinfectants, such as chlorine, react with natural organic matter and other precursors in the raw water. Over the past three decades, the potential health risks associated with DBPs have garnered significant attention, particularly since the discovery of chloroform in chlorinated drinking water.

Understanding Disinfection Byproduct Research

Research into the health effects of DBPs is multifaceted, primarily focusing on two key areas:

• Human Epidemiological Studies: These investigations analyze long-term health outcomes in populations exposed to disinfected drinking water, aiming to identify correlations between DBP exposure and specific health conditions. Such studies typically involve exposure to low DBP concentrations over many years.
• Laboratory Animal Studies: Conducted on animals, these studies evaluate the toxicity of individual DBPs and their mixtures. They often involve controlled exposure to various DBP concentrations to understand their mechanisms of action and potential health impacts.

Challenges in Laboratory Animal Research

Studying DBPs in laboratory animals presents several complexities:

• Diversity of DBPs: A vast number of DBPs can form, making comprehensive testing challenging.
• Varied Health Endpoints: Cancer, for instance, can manifest through diverse biological pathways.
• Species-Specific Responses: Different animal species may react dissimilarly to the same DBPs.

Despite these challenges, animal research often prioritizes DBPs with the highest human exposure rates and known toxicity.

Key Findings from Laboratory Animal Studies

• Reproductive Effects: Studies on laboratory rats indicate that bromodichloromethane (BDCM) and chloral hydrate (CH) can reduce sperm speed and mobility. BDCM, even at low concentrations, showed a stronger effect than CH or other tested DBPs. (Klinefelter, 1996)
• Carcinogenicity of DBP Mixtures: A 2002 study exposed Eker rats (known for sensitivity to renal carcinogens) to mixtures of dichloromethylhydroxyfuranone (MX), potassium bromate (KBrO$_3$), chloroform (CHCl$_3$), and bromodichloromethane (BDCM) in drinking water for 4 to 10 months. These DBPs were selected for their proven renal carcinogenic or nephrotoxic properties. While a dose-response relationship for renal cancer was observed, the study found no significant difference in tumor rates in kidneys, uterus, or spleen between rats exposed to the mixture versus the single DBP with the strongest effect. This suggests that the combined effect of these specific DBPs was not greater than the most potent individual DBP. (Hooth, 2002)
• Effects of Chlorine Dioxide, Chlorite, and Chlorate: A review of studies on rats, mice, and chickens exposed to chlorine dioxide, chlorite, and chlorate in drinking water revealed alterations in blood cells at high concentrations (up to 1 g/L or 1000 mg/L for chlorine dioxide; up to 100 mg/L for sodium chlorite/chlorate). Specifically, chlorite concentrations of 100 mg/L (100,000 µg/L) or more led to decreased red blood cells and hemoglobin. These effects often diminished after prolonged exposure (e.g., 90 days). Additionally, these compounds were shown to alter DNA in testes and kidneys, potentially impacting reproduction, though direct extrapolation to humans requires further research. (Couri, 1982)
• Chloroform Toxicity: Chloroform, a well-studied trihalomethane, causes liver damage and cancer in laboratory animals when large doses are directly administered to the stomach daily. This is attributed to the liver's inability to fully metabolize such high concentrations, leading to cell death and regenerative cell growth, increasing the risk of mutation and cancer. However, when animals were exposed to the same amount of chloroform dissolved in drinking water, cancer did not develop. This difference is likely due to the gradual intake over the day, allowing the liver to process smaller amounts without significant damage. The U.S. Environmental Protection Agency (EPA) concludes that cancer risk from chloroform is very low as long as exposure remains below thresholds that cause cell damage, a level far exceeding typical drinking water standards. (Larson, 1994a; Larson et al., 1994b; Butterworth et al., 1998; EPA, 1998)

Human Health Effects of Disinfection Byproducts

Beyond animal studies, extensive epidemiological research investigates the impact of DBP exposure on human health, primarily focusing on cancer and reproductive/developmental effects.

Carcinogenic Effects

Early studies in the 1960s, aided by advancements in analytical chemistry, identified a multitude of organic substances in drinking water, including carcinogenic or mutagenic DBPs like trihalomethanes (chloroform, bromoform, dichloromethane, and dibromomethane) found in all chlorinated water.

• Challenges in Proving Causality: In 1991, the WHO's International Agency for Research on Cancer (IARC) concluded that definitively linking cancer development to chlorinated water is difficult due to the small risk, inaccuracies in DBP exposure estimation, and numerous confounding factors (e.g., smoking, diet, genetics, socioeconomic status). (Disinfectants and Disinfection Byproducts, WHO, 2001)

• Bladder and Anal Cancer:

  • A meta-analysis indicated a positive correlation between DBP exposure in drinking water and bladder and anal cancer. It estimated that 9% of bladder cancer cases and 15% of anal cancer cases annually (approximately 10,000 cases) could be attributed to chlorinated drinking water and DBPs. (Morris, 1992)
  • Studies in Colorado (1990-1991) showed that the risk of bladder cancer increased with years of exposure to chlorinated drinking water. After 30 years of exposure, the risk was 1.8 times higher than for unexposed individuals. (McGeehin, 1993)
  • Research in Ontario, Canada, found a link between long-term DBP exposure and bladder cancer, particularly with trihalomethane (THM) concentrations of 50 µg/L (0.05 mg/L) or more. This study attributed 14-16% of all bladder cancer cases to DBP exposure. (King, 1996)
  • Finnish research found a significant connection between exposure to mutagenic and carcinogenic substances in drinking water and bladder cancer for both men and women, and renal cancer for men. (Koivusalo, 1998)
  • While individual risk may be small, the widespread and long-term exposure of populations to chlorinated drinking water makes the overall public health impact of DBP-related bladder cancer significant. (Kogevinas, 2003)

• Intestinal Cancer:

  • Some studies, like one in Ontario, Canada, involving 5000 people, suggested an elevated risk of intestinal cancer (1.5 times higher) for individuals exposed to THM concentrations of 50 µg/L (0.05 mg/L) or more. (Marret & King, 1995)
  • However, other studies, such as one in Iowa, Canada (1998), found no elevated risk, highlighting inconsistencies potentially due to differing water compositions or other factors. (Mills, 1998)

• Anal Cancer: A study in Iowa, USA (1986-1989), found no elevated risk of intestinal cancer from long-term exposure to chlorinated drinking water or THMs, but did identify an elevated risk for anal cancer, especially for individuals with low fibrous food intake and lack of physical exercise. (Hildesheim, 1998)

Reproductive and Developmental Effects

While cancer often receives more attention, DBPs may also impact human reproduction and development. Laboratory tests have shown that DBP exposure during pregnancy can influence reproduction and development, leading to birth defects and spontaneous abortion, typically at concentrations much higher than those causing cancer from long-term exposure. (Singer, 1999)

• Trihalomethanes (THMs): Epidemiological studies, though few, indicate a connection between THM exposure and spontaneous abortion, birth defects, and growth delay. (Wigle, 1998)
• Chlorine Dioxide Byproducts (Chlorite, Chlorate):
  • An early study in two communities, one using chlorine and the other chlorine dioxide for disinfection, found a significant link between maternal exposure to chlorine dioxide-treated water during pregnancy and premature birth and low birth weight. (Tuthill, 1982)
  • Conversely, a Norwegian study (1993-1995) of 137,145 births found no connection between exposure to chlorinated drinking water (even with high organic matter) and low birth weight or small body length. It even suggested a slightly smaller risk of premature birth with chlorinated water compared to non-chlorinated. (Jaakkola, 2001)
  • Research in Italy (1988-1989) found a correlation between drinking water disinfected with chlorine dioxide and smaller infant body length and cranial span, potentially linked to decreased maternal immunity. However, this study's conclusions are questioned due to unmeasured DBP concentrations and common bottled water consumption. (Kanitz, 1996)
• Birth Defects:
  • A Norwegian study (1993-1998) of 285,631 births found associations between DBP exposure during pregnancy and heart, breathing, and urine tract defects, with a significant increase in abdominal wall defects at higher exposures. (Bing-Fang, 2002)
  • Massachusetts data (1990) for 56,513 births showed THM concentrations of 80 µg/L (0.08 mg/L) or more were associated with a 32-gram reduction in birth weight and smaller body length (fetal growth delay), but no link to premature birth. (Wright, 2003)
  • Research in Nova Scotia, Canada (1988-1995), indicated that bromodichloromethane concentrations of 20 µg/L (0.02 mg/L) or more during pregnancy were linked to an elevated risk of neural tube defects, and chloroform exposure to an elevated risk of chromosomal defects. (Dodds, 2001)
  • A Swedish study (2001) of 59,422 children found an elevated risk of heart and artery defects when both chlorine dioxide and hypochlorite were used, suggesting that chlorine dioxide might increase this risk, even when THM levels were below standard limits. (Cedergren, 2001)
• Reliability of Reproduction Studies: Many studies show a probable link between exposure to chlorinated DBPs during pregnancy and birth defects, particularly low birth weight and growth delay. However, evidence for spontaneous abortion, specific birth defects, and still-birth is often inconsistent and lacks a strong dose-effect relationship. This may be due to varied research methods and challenges in accurately determining individual exposure. (Graves, 2001; Nieuwenhuijsen, 2000) More precise measurements of DBP concentrations at the tap, accounting for seasonal and annual variations, are needed. (Reif, 1996)

Recommendations for Disinfection Byproduct Control

The primary objective of water treatment remains the provision of microbiologically safe drinking water. The acute risk from pathogenic microorganisms in inadequately disinfected water is orders of magnitude higher (100,000 to 1,000,000 times) than the long-term risk from typical DBP concentrations. For example, the 1991 cholera epidemic in Peru, caused by insufficient disinfection, resulted in 1.2 million cases and 40,000 deaths across South America. (WHO, 1994)

Nevertheless, DBP risks, though low, cannot be ignored due to widespread exposure. Continuous research is needed to identify uncharacterized DBPs, assess their individual and combined health effects, and understand their mutagenic potential.

Control Methods for Disinfection Byproducts

Effective DBP control strategies aim to minimize their formation without compromising disinfection efficacy:

1. Pre-Disinfection Organic Matter Removal: This is the most effective approach. Removing natural organic matter (NOM) before disinfectant application reduces the available precursors for DBP formation. Techniques include:
   • Coagulation/Flocculation: To remove particles and turbidity.
   • Activated Carbon: To adsorb organic substances.
   • Membrane Filtration: To physically remove organic matter.
2. Alternative Disinfectants: While all disinfectants form some byproducts, alternatives can reduce specific DBP classes. Options include:
   • Ozone
   • Chlorine Dioxide
   • Potassium Permanganate
   • Chloramines (though these can form nitrogenous DBPs)
3. Optimization of Disinfectant Application Point: Adjusting where and when disinfectants are added can minimize reaction time with precursors.
4. Post-Disinfection DBP Removal: In some cases, technologies can be applied after disinfection to remove DBPs already formed.

Regulatory Standards for Disinfection Byproducts

Regulatory bodies worldwide have established standards for DBP concentrations in drinking water to protect public health. Some DBPs, like chloroform, dibromochloromethane, and bromoform, are classified as probable carcinogens, while others, such as dichlorobromomethane, dichloroacetonitrile, and chloral hydrates, are considered possible carcinogens.

The U.S. EPA's Stage 1 Disinfectants and Disinfection Byproducts Rule (1998) also mandates the use of advanced coagulation to enhance organic matter removal, reflecting the importance of precursor control. (EPA, 2001)

Learn more about specific types of disinfection byproducts.

AquaChain Engineering Tip

Prioritize upstream treatment processes, such as enhanced coagulation or membrane filtration, to remove Natural Organic Matter (NOM) before primary disinfection. This proactive precursor removal strategy is often more cost-effective and environmentally sound than trying to remove DBPs after they have formed.

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Frequently Asked Questions

Q1: Why are Disinfection Byproducts (DBPs) a concern if disinfection is essential for safe drinking water?

A1: While disinfection is crucial for eliminating harmful pathogens, the chemicals used can react with natural organic matter to form DBPs. The concern arises from potential long-term health effects associated with DBP exposure, such as increased cancer risks and reproductive issues, even at low concentrations.

Q2: What are the primary health effects linked to DBP exposure in drinking water?

A2: Research primarily points to two categories of health effects:

1. Carcinogenic effects: Studies suggest links to bladder, anal, and potentially intestinal cancers.
2. Reproductive and developmental effects: These include associations with low birth weight, growth delay, premature birth, and certain birth defects.

Q3: How can water treatment facilities minimize the formation of DBPs?

A3: DBP formation can be minimized by several strategies, including:

1. Precursor Removal: Removing natural organic matter (NOM) before disinfection through processes like enhanced coagulation, activated carbon, or membrane filtration.
2. Alternative Disinfectants: Using disinfectants like ozone, chlorine dioxide, or chloramines, which produce different or fewer regulated DBPs compared to free chlorine.
3. Process Optimization: Adjusting the point of disinfectant application, contact time, and pH to reduce DBP formation while maintaining effective pathogen kill.