Objectives: To evaluate the health risks associated with benzene exposure in elderly subjects following a flaring disaster at the BP refinery in Texas City, Texas.
Methods: Elderly subjects aged 60 years and older who had been exposed and unexposed to benzene were included. We reviewed medical charts and compared measures of white blood cells (WBC), platelets, hemoglobin, hematocrit, blood urea nitrogen (BUN), creatinine, alkaline phosphatase (ALP), aspartate amino transferase (AST), and alanine amino transferase (ALT) in exposed and unexposed elderly subjects.
Results: Records from 294 elderly subjects (benzene exposed, n=216 and unexposed, n=78) were reviewed. Benzene exposed subjects had significantly higher levels of WBC (X 103 per µL) (7.7±1.9 versus 6.3±1.5, P=0.0000) and platelet (X 103 per µL) counts (256.8 ± 51.6 versus 237.9 ± 41.9, P=0.0104) compared with the unexposed subjects. Serum creatinine levels (mg/dL) were also significantly increased in the exposed group compared with the unexposed group (1.1 ± 0.4 versus 0.9±0.2, P=0.000). Serum levels of ALP (IU/L) were significantly elevated in the exposed subjects compared with the unexposed subjects (87.5 ± 23.6 versus 72.5 ± 17.8, P=0.000). Similarly, benzene exposed subjects had significantly higher levels of AST (24.8 ± 6.2 versus 19.2 ± 5.1, IU/L, P=0.000) and ALT (24.2 ± 8.6 versus 19.1 ± 4.8, IU/L, P=0.000) compared with those unexposed to benzene.
Conclusions: Benzene exposure resulted in significant alterations in hematological and hepatic profiles among elderly subjects.
Petroleum refining industries are a major source of production of toxic chemicals such as benzene, toluene, and other volatile organic compounds in the environment(1). Benzene emission occurs most commonly during petroleum refinery operations(2). As a volatile organic compound, benzene is one of the major environmental contributors to air pollutants. It is found as a contaminant from both natural processes and human activities(3,4). Environmental contamination of benzene originates mainly from its industrial uses through improper discharge into the air. In addition, benzene is a commercially important intermediate chemical and used widely in the synthesis of various polymers, resins, and synthetic fibers. As a toxic pollutant, benzene is associated with significant health risks in communities surrounding petroleum refineries due to the increased probability of their exposure(5).
It is well established that human exposure to benzene is associated with increased risks of developing carcinogenesis, specifically, leukemia, lymphoma, and aplastic anemia(6,7,8,9,10). In addition, benzene exposure can cause a wide range of respiratory non-cancerous deleterious effects leading to impairment of the hematological, hepatic, renal, cardiovascular, neurological, and immune functions(11,12,13,14,15,16). Moreover, benzene exposure is associated with several adverse respiratory effects including pulmonary edema, acute granular tracheitis, laryngitis, bronchitis, and massive hemorrhaging(17,18). Benzene exposure can also affect both B-cell and T-cell proliferation, reduce host resistance to infections and produce chromosomal aberrations(19).
The adverse health effects of benzene exposure in adults have been well-documented and somewhat less in pediatric populations but not in elderly populations. Earlier studies have demonstrated that the elderly subjects are more susceptible to the effects of environmental pollutants than the young adult population(20,21). The increased susceptibility of elderly individuals to environmental pollutants could be due to normal and pathological aging and related processes. Normal aging in the elderly is associated with a progressive and inexorable loss of vital organ function leading to increased vulnerability to disease, frailty, and disability. In general, aging is accompanied by a gradual decline in the immune defense and functions leading to respiratory infections(22,23,24). Moreover, as the biologic capacity gradually declines with normal aging, these processes are exacerbated in pathologic aging. This decline can lead to compromised pharmacokinetic and pharmacodynamic responses to environmental pollutants. Furthermore, toxic exposure rates, absorption, metabolism, excretion, and tissue vulnerability all seem to be age-related(25) and thus, elderly individuals are more susceptible to the effects of environmental toxic pollutants. Thus, a better understanding of the health consequences faced by elderly populations following their exposure to toxic chemicals, particularly exposure to carcinogenic chemicals such as benzene is warranted.
In Texas City, Texas, a 2010 flaring disaster at the BP refinery facility lasted 40 days and led to the release of over 500,000 pounds of toxic chemicals, including over 17,000 pounds of benzene into the skies(26,27,28). Environmentally, this flaring disaster polluted the air with toxic emissions, especially benzene, and threatened the health of local communities living in close proximity to the BP refinery facility. To better understand more thoroughly the potential adverse health effects of the ambient benzene exposure resulting from the BP flaring disaster, we are conducting a series of studies by examining hematological and hepatic functions in children, adults, and elderly population following their exposure to benzene(29,30,31,32). The findings of these studies demonstrated that benzene exposure from the BP flaring disaster significantly altered the hematological and hepatic functions in the exposed populations. In this study, we investigated the health consequences of benzene exposure in elderly subjects after being exposed to the flaring disaster at the BP refinery facility.
SUBJECTS AND METHODS
This retrospective study was approved by an Institutional Review Board. The details of the subjects’ selection and the procedures employed for the clinical and laboratory evaluations were reported previously(29,30,31,32,33,34). Briefly, using medical charts, subjects who underwent clinical, as well as laboratory evaluations between June 2010 and October 2012, were included. The residential areas affected by the flaring disaster of the BP refinery facility were initially identified and the subjects exposed to the emissions were selected from the affected areas of the surrounding communities of Texas City, Texas (Figure 1). The subjects self-reported exposure to benzene following the flaring disaster from April 6, 2010, through May 16, 2010. Unexposed subjects were drawn from primary care clinics located approximately 30 – 50 miles away from the BP refinery plant. Unexposed subjects were individuals who visited the clinics for a routine wellness checkup. They were selected randomly by their primary care physicians. Only subjects (exposed and unexposed to benzene) aged 60 years or older were included in this study. Demographic and clinical laboratory data were reviewed and gathered for both benzene exposed and unexposed subjects and analyzed. The study was conducted according to the ethical principles of the Declaration of Helsinki. To comply with the Health Insurance Portability and Accountability Act (HIPAA), the confidentiality of information was secured by utilizing text encryption, password protection, and limited personnel involvement.