Can exposure to fuels, fumes, solvents, lubricants, and hydraulic fluids cause coronary artery disease and heart attacks?

Exposure to Fuels, Fumes, Solvents, Lubricants, and Hydraulic Fluids Causes Coronary Artery Disease and Heart Attacks

Yes, exposure to fuels, fumes, solvents, lubricants, and hydraulic fluids can cause coronary artery disease and heart attacks through multiple well-documented pathophysiological mechanisms. 1, 2 The evidence clearly demonstrates that these chemical exposures represent modifiable cardiovascular risk factors that can lead to both acute cardiac events and long-term cardiovascular disease.

Pathophysiological Mechanisms

Exposure to these industrial chemicals affects cardiovascular health through several key mechanisms:

• Autonomic nervous system disruption: Particulate matter from fuels and chemical fumes disrupts cardiac autonomic tone, affecting heart rate variability 1
• Endothelial dysfunction: Chemical exposures directly impair endothelial function and promote arterial stiffness 1
• Increased thrombogenicity: Particulate matter from fuels and exhaust can directly affect platelet activity and haemostasis, leading to increased risk of arterial and venous thrombotic events 2
• Myocardial ischemia: A randomized crossover study demonstrated significantly increased ischemic burden following exposure to diesel exhaust compared to filtered air 2, 1
• Reduced fibrinolytic activity: Exposure to diesel exhaust fumes reduces tissue plasminogen activator release, suggesting reduced endogenous fibrinolytic activity that may predispose to increased risk of myocardial infarction 2

Acute Cardiovascular Effects

The evidence shows both immediate and delayed effects of exposure:

• Short-term exposure to particulate matter has been associated with ventricular arrhythmias within 2 hours (OR = 1.31,95% CI: 1.00–1.72) 2
• Traffic exposure has been linked to a 2-3 fold increased risk of myocardial infarction within 1 hour of exposure 2, 1
• Higher levels of PM10 and NO2 have been associated with an increased risk of myocardial infarction 1-6 hours after exposure 2
• Exposure to diesel exhaust at 300 µg/m³ for just 2 hours resulted in arterial vasoconstriction, increased diastolic blood pressure, and decreased heart rate variability in susceptible individuals 3

Long-term Cardiovascular Effects

Chronic exposure to these chemicals contributes to:

• Development and progression of atherosclerosis 2
• Increased incidence of ischemic heart disease 2, 1
• Elevated risk of stroke 2
• Reduced life expectancy, with air pollution contributing to an average loss of 20 months of life expectancy globally 2

Occupational Exposure Risks

Workers in specific industries face heightened risks:

• Autoworkers exposed to oil-based metalworking fluids show increased cardiovascular mortality 4
• Shift workers with chemical exposures have a 40% increased risk of cardiovascular disease compared to day workers 2
• Aircraft crew exposed to hydraulic fluid fumes experience acute and long-term cardiovascular symptoms 5

Prevention and Management

To reduce cardiovascular risk from these exposures:

1. Workplace interventions:

   • Adherence to all regulations addressing hazards to employee health and safety 2
   • Implementation of environmental modifications in workplaces to reduce exposures 2
   • Use of appropriate respiratory protection 1

2. Personal protective measures:

   • Room air filtration in workplaces and residences has been shown to improve blood pressure and reduce inflammation 2, 1
   • Monitoring air quality indices to adjust activities during poor air quality periods 2, 1

3. Clinical approach:

   • Healthcare providers should integrate exposure assessment into cardiovascular disease management 1
   • Clinicians should advocate for air pollution mitigation as a health measure 2
   • Detailed air pollution maps can be used to target cardiovascular disease treatment in those with highest exposures 2

Regulatory Considerations

The American Heart Association, American College of Cardiology, European Society of Cardiology, and World Heart Federation have jointly called for:

• Recognition of air pollution and chemical exposures as modifiable cardiovascular risk factors 2, 1
• Development of clinical guidelines on air pollution and cardiovascular disease 2
• Regulatory provisions providing wellness credits for employers who implement healthy workplace interventions 2

Common Pitfalls and Caveats

• Delayed effects: The cardiovascular impact of exposure may not be immediate but can occur hours after exposure ends, making the connection less obvious 2
• Cumulative exposure: Regular exposure to small doses of toxic fumes can cause cumulative damage, potentially exacerbated by a single higher-level exposure 5
• Complex mixtures: Assessment is complicated because most exposures involve complex mixtures of chemicals rather than single substances 5
• Individual susceptibility: Genetic factors (like GSTM1 null genotype) may increase susceptibility to cardiovascular effects of these exposures 3

The evidence clearly establishes that exposure to fuels, fumes, solvents, lubricants, and hydraulic fluids represents a significant and modifiable risk factor for coronary artery disease and heart attacks through multiple pathophysiological mechanisms.