Fatty liver disease and Camp Lejeune water contamination represent two distinct but potentially intersecting health concerns. Between the 1950s and 1987, approximately one million people at Camp Lejeune, a US Marine Corps base, were exposed to drinking water contaminated with industrial chemicals including trichloroethylene and perchloroethylene. Whilst these volatile organic compounds have demonstrated hepatotoxic properties in animal studies, no official link has been definitively established between Camp Lejeune exposure and fatty liver disease in humans. This article examines the evidence surrounding environmental chemical exposure and liver health, explores the pathophysiology of fatty liver disease, and provides guidance for affected individuals seeking medical evaluation and support within UK and US healthcare systems.

Understanding Fatty Liver Disease: Causes and Risk Factors

Fatty liver disease, medically termed hepatic steatosis, occurs when excess fat accumulates within liver cells. Clinically, it is defined as steatosis affecting more than 5% of hepatocytes, as determined by histology or equivalent imaging criteria. This condition exists in two primary forms: non-alcoholic fatty liver disease (NAFLD), which develops independently of alcohol consumption, and alcoholic fatty liver disease, directly related to excessive alcohol intake. (International terminology is evolving towards metabolic dysfunction-associated steatotic liver disease [MASLD], though UK guidance currently uses NAFLD.)

The pathophysiology of NAFLD involves complex metabolic dysfunction. When the liver receives more fatty acids than it can process through oxidation or export as lipoproteins, triglycerides accumulate within hepatocytes. This process is frequently associated with insulin resistance, where cells become less responsive to insulin signalling, leading to increased hepatic fat deposition.

Established risk factors for fatty liver disease include:

• Metabolic conditions – Type 2 diabetes mellitus, obesity (particularly central adiposity), dyslipidaemia, and metabolic syndrome

• Lifestyle factors – Sedentary behaviour, high-calorie diets rich in refined carbohydrates and saturated fats

• Medications – Certain drugs including corticosteroids, amiodarone, tamoxifen, methotrexate, valproate, and some antiretroviral agents

• Genetic predisposition – Variations in genes such as PNPLA3 and TM6SF2

NAFLD is common in the UK, affecting a substantial proportion of the adult population, though many individuals have early, asymptomatic disease. Emerging research explores whether environmental toxicant exposure may contribute to liver disease development. Certain industrial chemicals and contaminants have demonstrated hepatotoxic properties in experimental studies, though establishing causation in human populations remains methodologically challenging. The liver's role as the body's primary detoxification organ makes it particularly vulnerable to chemical injury, as hepatocytes metabolise and process xenobiotic compounds. Understanding these diverse aetiological factors is essential for comprehensive risk assessment and prevention strategies, as outlined in NICE guidance (NG49).

Camp Lejeune Water Contamination: What Happened

Camp Lejeune, a United States Marine Corps base in North Carolina, experienced one of the largest documented water contamination incidents in American history. Between the 1950s and 1987, an estimated one million military personnel, their families, and civilian workers were potentially exposed to contaminated drinking water supplies at the installation.

The contamination involved multiple volatile organic compounds (VOCs) at concentrations substantially exceeding US Environmental Protection Agency (EPA) safe drinking water standards. Primary contaminants identified included:

• Trichloroethylene (TCE) – An industrial degreasing solvent, detected at peak concentrations up to approximately 1,400 micrograms per litre (µg/L), compared with the US EPA maximum contaminant level (MCL) of 5 µg/L

• Perchloroethylene (PCE) – A dry-cleaning chemical found at concentrations up to approximately 215 µg/L, compared with the MCL of 5 µg/L

• Benzene – A known human carcinogen present at levels up to approximately 700 µg/L, compared with the MCL of 5 µg/L

• Vinyl chloride – Another carcinogenic compound formed through PCE degradation, detected at levels up to approximately 22 µg/L, compared with the MCL of 2 µg/L

The contamination sources were traced to on-base industrial activities, including improper disposal practices at dry-cleaning facilities and leaking underground storage tanks. Two primary water treatment plants, Tarawa Terrace and Hadnot Point, supplied the affected water to residential areas, barracks, schools, and medical facilities throughout the base.

The United States government formally acknowledged the contamination in the 1980s, and subsequent epidemiological investigations by the Agency for Toxic Substances and Disease Registry (ATSDR) have examined potential health consequences. In 2012, the Camp Lejeune Veterans and Family Members Act provided healthcare benefits to affected individuals. Whilst this incident occurred in the United States, it serves as an important case study in environmental health, illustrating how industrial chemical exposure can affect large populations and highlighting the importance of water quality monitoring and environmental protection standards globally.

Link Between Toxic Exposure and Liver Disease

The relationship between environmental chemical exposure and liver disease represents an evolving area of toxicological and epidemiological research. The liver's central role in xenobiotic metabolism makes it a primary target organ for chemical-induced injury, as hepatocytes contain high concentrations of cytochrome P450 enzymes that biotransform foreign compounds.

Trichloroethylene (TCE) and perchloroethylene (PCE), the predominant contaminants at Camp Lejeune, undergo hepatic metabolism producing reactive intermediates. Animal studies have demonstrated that chronic TCE exposure can induce hepatic steatosis, inflammation, and oxidative stress. The proposed mechanisms include disruption of lipid metabolism, mitochondrial dysfunction, and interference with peroxisome proliferator-activated receptors (PPARs) that regulate fatty acid oxidation. The International Agency for Research on Cancer (IARC) classifies TCE as a Group 1 carcinogen (carcinogenic to humans) and PCE as a Group 2A carcinogen (probably carcinogenic to humans), reflecting their hazard profiles.

However, establishing a definitive causal link between Camp Lejeune water contamination and fatty liver disease in exposed individuals remains scientifically complex. Epidemiological studies face challenges including long latency periods, difficulty quantifying historical exposure levels, and the multifactorial nature of liver disease. The ATSDR has conducted health studies on Camp Lejeune populations, identifying associations with certain cancers and other conditions, though liver disease has not been conclusively established as a presumptive condition.

It is important to note that there is no official link definitively proven between Camp Lejeune water exposure and fatty liver disease specifically. Current evidence suggests biological plausibility based on toxicological mechanisms, but human epidemiological data remain limited. The UK Health Security Agency (UKHSA) and Health and Safety Executive (HSE) recognise that occupational and environmental chemical exposures can contribute to liver injury, though individual risk assessment requires consideration of exposure duration, concentration, and personal susceptibility factors. Anyone concerned about potential exposure-related health effects should seek medical evaluation for proper assessment.

Symptoms and Diagnosis of Fatty Liver Disease

Fatty liver disease frequently presents asymptomatically, particularly in early stages, earning it recognition as a 'silent' condition. Many individuals remain unaware of hepatic steatosis until incidental discovery through imaging performed for unrelated reasons or during routine health assessments. When symptoms do manifest, they tend to be non-specific and may include persistent fatigue, malaise, or vague right upper quadrant discomfort.

As the condition progresses to non-alcoholic steatohepatitis (NASH), where inflammation accompanies fat accumulation, patients may experience more pronounced symptoms including hepatomegaly (enlarged liver), jaundice (in advanced cases), and signs of portal hypertension if cirrhosis develops.

Diagnostic approach follows NICE guidance (NG49) and typically includes:

Initial assessment:

• Comprehensive medical history, including alcohol consumption, medication review, and metabolic risk factors

• Physical examination assessing for hepatomegaly, stigmata of chronic liver disease

• Blood tests – Liver function tests (ALT, AST, GGT, ALP, bilirubin, albumin), fasting glucose and lipid profile, full blood count, and screening for viral hepatitis

Imaging investigations:

• Ultrasound scanning – First-line imaging modality demonstrating increased hepatic echogenicity

• Transient elastography (FibroScan) – Non-invasive assessment of liver stiffness to evaluate fibrosis

• MRI – Reserved for complex cases or when alternative diagnoses are considered (CT is not routinely used for steatosis assessment due to radiation exposure)

Fibrosis risk stratification:

Non-invasive scoring systems are used to stratify patients according to fibrosis risk. The FIB-4 index or NAFLD fibrosis score are first-line tools. Age-adjusted cut-offs are important: for adults under 65 years, a FIB-4 score below 1.3 generally rules out advanced fibrosis, whilst a score above 2.67 indicates high risk and prompts referral or second-line testing. For adults aged 65 and over, higher thresholds (e.g., around 2.0 for rule-out) may be considered to reduce false positives. Indeterminate scores warrant second-line assessment with the Enhanced Liver Fibrosis (ELF) test; an ELF score of 10.51 or above suggests advanced fibrosis and warrants referral to hepatology services.

Liver biopsy, whilst the gold standard for definitive diagnosis and staging, is typically reserved for cases where non-invasive methods are inconclusive or when alternative diagnoses require exclusion. There is no national screening programme for NAFLD in the UK; instead, opportunistic case-finding is recommended in high-risk groups, such as individuals with type 2 diabetes or metabolic syndrome. Early detection through systematic case-finding enables timely intervention before irreversible liver damage occurs.

Treatment Options and Liver Health Management

Management of fatty liver disease centres on addressing underlying metabolic dysfunction and preventing disease progression. Currently, no pharmacological agents hold specific UK marketing authorisation for NAFLD treatment, making lifestyle modification the cornerstone of therapeutic intervention.

Evidence-based management strategies include:

Weight reduction and dietary modification:

Gradual, sustained weight loss of 7–10% body weight has demonstrated significant improvements in hepatic steatosis and inflammation. NICE recommends a balanced, calorie-controlled diet emphasising whole grains, lean proteins, fruits, vegetables, and healthy fats whilst limiting refined carbohydrates, saturated fats, and added sugars. Mediterranean dietary patterns show particular promise in improving liver health markers. Structured weight management programmes, and where clinically indicated, GLP-1 receptor agonists for obesity or type 2 diabetes, and bariatric surgery (according to NICE criteria), may be considered.

Physical activity:

Regular aerobic exercise (150 minutes weekly of moderate-intensity activity, as per UK Chief Medical Officers' guidelines) and resistance training improve insulin sensitivity and reduce hepatic fat content, even independent of weight loss. The NHS recommends incorporating movement throughout daily routines alongside structured exercise sessions.

Management of comorbidities:

Optimal control of type 2 diabetes, hypertension, and dyslipidaemia is essential. Metformin, whilst not specifically indicated for NAFLD, benefits patients with concurrent diabetes. Statins are safe in fatty liver disease and should be prescribed according to cardiovascular risk assessment guidelines (NICE NG238).

Pharmacological considerations:

Vitamin E (800 IU daily) and pioglitazone may benefit selected adults with biopsy-proven NASH, but both are off-label uses in the UK and should only be initiated under specialist hepatology supervision. Vitamin E carries risks including haemorrhagic stroke and a possible increased risk of prostate cancer in some populations; long-term safety requires careful consideration. Pioglitazone is associated with weight gain, fluid retention (with risk of heart failure exacerbation), increased fracture risk, and a possible signal for bladder cancer. These agents are not suitable for all patients, and decisions must be individualised. Emerging therapies are under investigation but not yet routinely available.

Alcohol consumption:

Patients should be advised to stay within the UK Chief Medical Officers' low-risk drinking guidelines (no more than 14 units per week, spread over at least three days, with several alcohol-free days). Complete abstinence is recommended for individuals with advanced fibrosis or cirrhosis, or as advised by a hepatologist.

Vaccination:

Individuals with chronic liver disease should be offered hepatitis A and hepatitis B vaccination in accordance with the UK immunisation schedule (Green Book).

Monitoring and follow-up:

Regular assessment of liver function, metabolic parameters, and fibrosis progression (using non-invasive tools such as FIB-4 and ELF where appropriate) guides ongoing management. Patients should be counselled about red flag symptoms warranting urgent medical attention: jaundice, ascites, confusion, or gastrointestinal bleeding. Referral to hepatology services is appropriate for advanced fibrosis (e.g., ELF ≥10.51), diagnostic uncertainty, or inadequate response to initial interventions.

Reporting side effects:

If you experience side effects from any medicine, report them via the MHRA Yellow Card scheme at yellowcard.mhra.gov.uk or through the Yellow Card app.

Support for Camp Lejeune Veterans and Affected Individuals

Individuals who lived or worked at Camp Lejeune during the contamination period may access specific support mechanisms, though these primarily operate within the United States healthcare and legal systems. Understanding available resources is important for affected persons, including UK residents who may have been stationed at the base during military service or as dependents.

Healthcare provisions:

The United States Department of Veterans Affairs (VA) provides healthcare benefits to eligible veterans and family members who resided at Camp Lejeune for at least 30 days between August 1953 and December 1987. Covered conditions include certain cancers, neurological disorders, and other specified illnesses, though the list of presumptive conditions continues to evolve as research progresses.

Legal recourse:

The Camp Lejeune Justice Act of 2022 created a pathway for affected individuals to pursue compensation claims for health conditions potentially linked to water contamination exposure. This legislation allows civil actions in United States federal court, though establishing causation for specific conditions requires substantial medical documentation. (This information is provided for context and does not constitute legal advice.)

For UK-based individuals:

British military personnel or dependents who were stationed at Camp Lejeune should contact Veterans UK, part of the Ministry of Defence, for guidance on accessing appropriate support. The Veterans Welfare Service can provide advice on navigating both UK and US systems. Contact details and further information are available at gov.uk/government/organisations/veterans-uk. NHS care remains available for all health concerns, with GPs able to refer to hepatology services when liver disease is suspected.

Medical documentation:

Individuals concerned about potential exposure-related health effects should maintain comprehensive medical records, document their residence dates at Camp Lejeune, and discuss their exposure history with healthcare providers. Whilst there is no official link established between Camp Lejeune contamination and fatty liver disease specifically, thorough medical evaluation of any liver abnormalities is warranted. Specialist hepatology assessment can determine whether liver disease is present and guide appropriate management regardless of aetiology. Support groups and advocacy organisations provide additional resources for affected communities navigating these complex health and administrative challenges.

Frequently Asked Questions