Benzethonium is also
a from of benzene.
This is a component in the HIV and AIDS drugs (AZT) attacks the thymus. Your
thymus responsibile for manufacturing your T4 cells. These are your killer cells
responsible for attacking dangerous negative bacterium and viruses. Eventually,
after so much invasion from the benzene, the production of your T4 killer cells by the
thymus is seriously disrupted. This disruption, if not fixed, literally lead to AIDS
(auto immune difficiency syndrome) as a result of the body no longer able to fight
anything that comes it's way.
thymus (located in the upper chest or base of the neck)
Benzene primarily affects the CNS and the hematopoietic
system.
Benzene exposure affects the CNS and hematopoietic
system and may affect the immune system. Death due to acute benzene exposure has been
attributed to asphyxiation, respiratory arrest, CNS depression, or cardiac dysrhythmia.
Pathologic findings in fatal cases have included respiratory tract inflammation, lung
hemorrhages, kidney congestion, and cerebral edema.
At very high concentrations, benzene rapidly causes
CNS depression, which can lead to death.
Acute benzene exposure results in classic symptoms
of CNS depression such as dizziness, ataxia, and confusion. These effects are believed to
be caused by benzene itself rather than its metabolites, because the onset of CNS effects
at extremely high doses is too rapid for metabolism to have occurred.
All three blood cell lines may be adversely affected
by benzene.
Pluripotential stem cells and lymphocytic cells are
the probable targets of benzene toxicity.
Benzene can cause dangerous hematologic toxicity
such as anemia, leukopenia, thrombocytopenia, or pancytopenia after chronic exposure.
These effects are believed to be caused by the metabolites of benzene, which most likely
damage the DNA of the pluripotential stem cells. All of the blood's components (i.e.,
erythrocytes, leukocytes, and thrombocytes [platelets]) may be affected to varying
degrees. The accelerated destruction or reduction in the number of all three major types
of blood cells is termed pancytopenia. Potentially fatal infections can develop if
granulocytopenia is present, and hemorrhage can occur as a result of thrombocytopenia.
Paroxysmal nocturnal hemoglobinuria, a disorder in which the breakdown of the red blood
cells is accelerated and results in bleeding into the urine during sleep when the
condition is active, has been associated with benzene exposure. Cytogenetic abnormalities
of bone marrow cells and circulating lymphocytes have been observed in workers exposed to
benzene—abnormalities not unlike those observed after exposure to ionizing radiation.
Myelodysplastic effects also can be seen in the bone marrow of persons chronically exposed
to benzene.
Benzene-induced aplastic anemia is caused by chronic
exposure at relatively high levels.
Aplastic anemia is caused by bone marrow failure,
resulting in hypoplasia with an inadequate number of all cell lines. Severe aplastic
anemia typically has a poor prognosis and can progress to leukemia, whereas pancytopenia
may be reversible. Benzene-induced aplastic anemia is generally caused by chronic exposure
at relatively high doses. Fatal aplastic anemia following benzene exposure was first
reported in workers in the nineteenth century.
Benzene-induced leukemia has a usual latency period
of 5 to 15 years and, in many cases, is preceded by aplastic anemia.
Several agencies (e.g., the U.S. Department of
Health and Human Services, the U.S. Environmental Protection Agency [EPA], and the
International Agency for Research on Cancer) classify benzene as a confirmed human
carcinogen. EPA estimates that a lifetime exposure to 4 ppb benzene in air will result in,
at most, 1 additional case of leukemia in 10,000 people exposed. EPA has also estimated
that lifetime exposure to a benzene concentration of 100 ppb in drinking water would
correspond to, at most, 1 additional cancer case in 10,000 people exposed.
Cohort studies of benzene-exposed workers in several industries (e.g., sheet-rubber
manufacturing, shoe manufacturing, and rotogravure [a special printing process]) have
demonstrated significantly elevated risk of leukemia—predominantly acute myelogenous
leukemia, but also erythroleukemia and acute myelomonocytic leukemia. The latency period
for benzene-induced leukemia is typically 5 to 15 years after first exposure. Patients
with benzene-induced aplastic anemia progress to a preleukemic phase and develop acute
myelogenous leukemia. However, a person exposed to benzene may develop leukemia without
having aplastic anemia.
Studies addressing the risk of leukemia associated with occupational exposures to low
levels of benzene (less than approximately 1 ppm) have been inconclusive. Death
certificates do not reveal increased leukemia mortality among workers potentially exposed
to low levels of hydrocarbons and other petroleum products.
However, in recent case-control studies,
significantly more patients with acute nonlymphocytic leukemia were employed as truck
drivers, filling station attendants, or in jobs involving exposure to low levels of
petroleum products than were the controls.
